New-onset seizures in a malnourished adolescent with chronic recurrent abdominopelvic pain: a case report

Introduction

Chronic abdominal or abdominopelvic pain is a frequent reason for emergency department (ED) visits and recurrent hospitalizations. It becomes clinically difficult when routine imaging, endoscopic evaluation, and laboratory testing do not identify a visceral cause. In this setting, clinicians may prematurely attribute symptoms to a disorder of gut-brain interaction or pursue rare diagnoses before more likely and reversible causes have been weighed carefully. A systematic approach based on history, physical examination, alarm features, and targeted testing has been recommended to reduce unnecessary investigations while minimizing missed serious disease (1,2).

When recurrent abdominal pain coexists with new-onset seizures, the differential diagnosis broadens. Acute hepatic porphyrias (AHPs), autoimmune encephalitis, structural brain disease, toxic-metabolic disturbances, and primary epileptic syndromes may all be considered (3,4). Acute symptomatic seizures should be assessed early, particularly when electrolyte abnormalities are present, because disturbances in sodium, calcium, and magnesium are recognized and potentially reversible seizure precipitants (5,6). Seizure phenotyping is also relevant because distinguishing focal, generalized, and unknown-onset seizures guides antiseizure medication selection and may prevent the use of agents poorly suited to a given electroclinical pattern (7,8).

Abdominal epilepsy is uncommon and generally refers to epileptic events with prominent autonomic or visceral manifestations, including epigastric discomfort, nausea, vomiting, or abdominal pain. Previous reports have described patients with recurrent unexplained abdominal symptoms, abnormal electroencephalographic findings, and improvement after antiseizure therapy (9-13). However, abdominal symptoms are not specific to epilepsy. They may occur as peri-ictal symptoms, coexist with gastrointestinal disorders, or reflect metabolic, inflammatory, infectious, toxic, or structural disease. For this reason, abdominal epilepsy should not be considered confirmed unless the clinical pattern, diagnostic work-up, electroencephalographic findings, and treatment response are interpreted together; whenever feasible, video-electroencephalographic capture of a typical abdominal event provides the strongest support.

We present a diagnostically challenging case of new-onset seizures in a malnourished adolescent with chronic recurrent abdominopelvic pain. The case reflects a bedside problem: how far to attribute seizures to correctable metabolic abnormalities, and when to continue investigating recurrent abdominal events as potentially neurological. We present this article in accordance with the CARE reporting checklist (available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-2026-0009/rc).

Case presentation

A 19-year-old woman from rural Filadelfia, Caldas, Colombia, was referred to the ED on October 16, 2025, for worsening recurrent abdominopelvic pain. She was accompanied by her mother, and the information was considered reliable. The available records described a 5-year history of chronic recurrent abdominal pain with previous hospitalizations. The pain was disabling, with paroxysmal exacerbations described as severe, colicky, stereotyped, and abrupt in onset and offset. During these episodes she reported abdominal wall stiffening with preserved awareness; the events usually lasted several hours and were followed by functional limitation.

The relationship with menstruation was inconsistent. She denied dyspareunia, reproducible triggers, bowel or urinary symptoms, fever, respiratory complaints, chest pain, palpitations, focal neurologic deficits, behavioral change, relevant travel, vector exposure, toxic exposure, or similar symptoms among close contacts. Her history included polycystic ovary syndrome, major depressive disorder, appendectomy, and ovarian cystectomy for adnexal torsion. Home medications included carbamazepine, escitalopram, and quetiapine.

On arrival, she was tachycardic but hemodynamically stable. She weighed 39 kg, measured 1.51 m, and had a body mass index of 17.1 kg/m². The abdomen was not distended and was diffusely tender, mainly in the hypogastrium and left iliac fossa, without peritoneal signs. Neurologic examination was non-focal. Initial evaluation showed a negative pregnancy test, normal complete blood count, preserved renal and hepatic function, sodium 138 mmol/L, total calcium 7.9 mg/dL, magnesium 1.5 mg/dL, low 25-hydroxyvitamin D, and normal parathyroid hormone (PTH). Arterial blood gas and lactate did not show major abnormalities. The main events and laboratory findings are summarized in Tables 1,2.

She was admitted to Hospital Santa Sofía. Initial treatment addressed pain, nausea, and psychiatric comorbidity. Because AHP was considered, dextrose infusion was started and porphobilinogen (PBG) testing was requested. Random and 24-hour urine PBG were reported as negative, and molecular testing for porphyria was later negative.

On October 21, 2025, she developed the first documented seizure-like event, described as upper-limb clonic movements, sphincter relaxation, tonic abdominal wall contraction, and post-event somnolence. Around this period, carbamazepine was discontinued by psychiatry, and escitalopram and quetiapine were continued or initiated. A neurological origin for the abdominal events was considered because of their abrupt and repetitive pattern, abdominal wall contraction during the documented event, and subsequent electroencephalographic abnormalities. However, no typical abdominal event was captured during video-electroencephalography (EEG).

Neuroimaging did not show structural lesions: non-contrast head computed tomography (CT) on October 22 was normal, brain magnetic resonance imaging (MRI) on October 25 was reported without abnormalities, and repeat imaging during later clinical deterioration was also unrevealing. A 6-hour video-EEG on October 30 showed generalized interictal epileptiform activity with scarce generalized spike/sharp-wave discharges at approximately 4 Hz, in brief paroxysms. Abdominal and gynecologic evaluation did not identify an acute visceral cause; contrast-enhanced abdominal CT on November 10 was within normal parameters except for an incidental right adnexal follicular-appearing image.

On November 23, she developed convulsive status epilepticus requiring intubation and intensive care. After stabilization, a neurology teleconsultation considered possible mesial temporal lobe epilepsy versus abdominal epilepsy and recommended antiseizure treatment. Recurrent seizures occurred, with the last pre-transfer episode documented on December 5 and controlled with benzodiazepines.

On December 6, she was transferred to Servicios Especiales de Salud for interdisciplinary neurological management. Electrocardiography showed sinus rhythm without ischemic changes, conduction block, or QT prolongation; no additional cardiac testing was performed. She received levetiracetam, valproate/divalproate, and lacosamide. Serum anti-N-methyl-D-aspartate (NMDA) receptor antibodies were requested because of concern for autoimmune encephalitis and were later negative. Lumbar puncture was not performed. Brain MRI with and without gadolinium on December 9 was normal, including cortex, white matter, basal nuclei, hippocampi, entorhinal cortex, brainstem, and cerebellum. She remained seizure-free during this admission and was discharged on December 11 after pharmacological adjustment.

She re-presented on January 14, 2026, with recurrent seizures after poor adherence to antiseizure therapy, including suspension of levetiracetam for several days. This readmission required intensive care for status epilepticus and was complicated by aspiration pneumonia, which resolved with ureidopenicillin therapy. Repeat head CT was normal. A 3- hour EEG on January 26 during sleep showed rare interictal bifrontal slow spike-and-wave elements, predominantly on the left (Figure 1). She was discharged after clinical stabilization on February 5.

Figure 1 Representative epoch from a 3- hour EEG performed on January 26, 2026, during sleep stages I–III, showing rare interictal bifrontal slow spike-and-wave complexes with left-sided predominance in a longitudinal bipolar 10–20 montage. EEG, electroencephalography.

All procedures performed in this study were in accordance with the Declaration of Helsinki and its subsequent amendments. This report describes a single clinical case, involved no experimental intervention, and all clinical information was de-identified. Institutional ethics committee approval was not required for this single-patient case report according to local institutional requirements. Written informed consent was obtained from the patient for publication of this case report and any accompanying clinical information and the image. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

The main challenge was not the recognition of seizures alone, but their interpretation in a malnourished adolescent with years of recurrent abdominopelvic pain. The case combined hypocalcemia, hypomagnesemia, low 25-hydroxyvitamin D, negative available testing for AHP, normal abdominal and brain imaging, and interictal epileptiform abnormalities. The abdominal events were stereotyped and abrupt, which raised the possibility of a neurological origin. However, no typical abdominal event was captured on video-EEG, and the prolonged duration of pain makes abdominal epilepsy uncertain rather than confirmed.

The case should not be read as proof of abdominal epilepsy. Its value is more practical: it shows how an epileptic explanation may enter the differential while reversible metabolic factors still require priority. Labeling the presentation too early as abdominal epilepsy may shift attention away from correctable metabolic factors; dismissing the abdominal events entirely may also delay neurological evaluation.

Strengths and limitations

Several elements strengthen the clinical description, including longitudinal documentation across two admissions, seizure evolution, intensive care escalation, follow-up EEG, and later status epilepticus in the setting of poor adherence. The work-up also addressed major competing diagnoses through PBG testing, abdominal CT, brain CT, brain MRI, electrocardiography, and serial electroencephalographic assessments.

The limitations are equally important. A typical abdominal event was not captured on video-EEG, preventing confirmation of abdominal epilepsy. Lumbar puncture was not performed, so inflammatory or autoimmune central nervous system disorders cannot be definitively excluded, although there was no persistent fever, meningismus, or sustained encephalopathy. Inflammatory bowel disease and other chronic gastrointestinal disorders were not systematically excluded with fecal calprotectin, inflammatory markers, colonoscopy, or dedicated gastroenterology testing. Cardiac evaluation was limited to electrocardiography, which restricts exclusion of intermittent arrhythmic or syncopal mimics. Finally, metabolic correction, sedative infusions, and multiple antiseizure medications overlapped, so stabilization cannot be attributed to antiseizure therapy alone.

Comparison with similar reports

Previous reports of abdominal epilepsy describe recurrent unexplained abdominal pain, abnormal electroencephalographic findings, delayed neurological recognition, and improvement after antiseizure medication (9-13). This case shares several features with that literature, including chronic abdominal symptoms, unrevealing abdominal imaging, interictal epileptiform abnormalities, and later overt seizures. It differs in clinically important ways: the patient had malnutrition, hypocalcemia, hypomagnesemia, and low vitamin D, all of which could precipitate acute symptomatic seizures; the abdominal events lasted hours, which is not typical for most focal seizures; and the electroencephalographic abnormalities were interictal and generalized or bifrontal rather than a captured focal ictal correlate. The report therefore adds value because of its uncertainty: the same findings that made an epileptic explanation plausible coexisted with metabolic abnormalities that could explain the new-onset seizures.

Explanations of findings

The early electrolyte abnormalities should not be treated as incidental. In a malnourished patient, hypocalcemia, hypomagnesemia, and low vitamin D may lower the seizure threshold (5,6). Hypomagnesemia can impair PTH secretion and action, making hypocalcemia more difficult to correct until magnesium is repleted (14). This mechanism makes the metabolic abnormalities a potentially sufficient explanation for the first documented seizures.

AHP was appropriate to consider because it can present with severe abdominal pain, normal imaging, neuropsychiatric manifestations, and seizures (3). In this case, random and 24-hour urine PBG were negative, and molecular testing was later negative. Although biochemical testing remains the key initial test during symptomatic periods, these findings lowered the probability of AHP (3).

Autoimmune encephalitis was also considered because new-onset seizures can be part of its presentation (4). Serum anti-NMDA receptor antibodies were negative; however, absence of cerebrospinal fluid analysis still limits exclusion of autoimmune encephalitis. Even so, the chart did not document a clear subacute encephalitic syndrome, making autoimmune encephalitis a less immediate explanation in the available clinical narrative.

Interictal epileptiform discharges increase the likelihood of an epileptic disorder and help refine seizure classification (7,8). In this patient, generalized interictal discharges and later bifrontal slow spike-and-wave elements supported neurological follow-up and broad-spectrum antiseizure therapy. They also supported avoiding or discontinuing narrow-spectrum sodium-channel agents such as carbamazepine when a generalized epilepsy phenotype was possible, because carbamazepine may worsen some generalized epilepsies (15,16).

Nevertheless, an abnormal interictal EEG does not prove that the abdominal events were seizures. Abdominal epilepsy is usually conceptualized as epileptic events with prominent autonomic or visceral manifestations, supported by clinical pattern, electroencephalographic abnormalities, exclusion of alternatives, and treatment response (9-13,17). Here, stereotyped abdominal events, abrupt onset and offset, abdominal wall contraction, abnormal interictal EEG, and recurrence during nonadherence raised suspicion. Against this interpretation are prolonged pain duration, lack of ictal electroclinical correlation, and metabolic abnormalities that could explain the new-onset seizures. Abdominal epilepsy is therefore best described as a high-suspicion clinical hypothesis, not a confirmed diagnosis.

Implications and actions needed

For emergency, internal medicine, neurology, and critical care teams, the practical message is straightforward. In patients with recurrent abdominal pain and new-onset seizures, clinicians should first identify and correct reversible metabolic and nutritional abnormalities. Neurological causes should remain in the differential when abdominal events are recurrent, stereotyped, abrupt, and unexplained by visceral evaluation. Early EEG is useful, but the strongest diagnostic step is capture of a typical abdominal event during video-EEG.

Cases like this require a stepwise work-up rather than early closure on a rare diagnosis. AHP should be assessed with urine PBG during symptoms; autoimmune encephalitis should prompt cerebrospinal fluid evaluation when suspicion is meaningful; structural brain disease requires adequate neuroimaging; and chronic gastrointestinal disorders, including inflammatory bowel disease, should be evaluated when symptoms or alarm features support that pathway. Antiseizure medication should be guided by seizure phenotype and electroencephalographic pattern, and adherence counseling is essential. In women of childbearing potential, valproic acid also requires careful risk-benefit discussion and reproductive counseling.

Conclusions

In neurovisceral presentations, clinicians should avoid early diagnostic closure around a rare entity and follow a stepwise approach. Rare diagnoses such as AHPs and autoimmune encephalitis should be considered, but correction of common reversible precipitants—particularly metabolic and nutritional abnormalities—should not be delayed (5,6). Seizure classification and electroencephalographic phenotyping help guide antiseizure medication selection and may prevent the use of agents poorly suited to a generalized epileptiform pattern (7,8,15,16). Abdominal epilepsy should remain in the differential when abdominal events are recurrent, stereotyped, abrupt, and unexplained by visceral evaluation (9-13). In this patient, however, the diagnosis could not be confirmed because no typical abdominal event was captured on video-EEG, and metabolic abnormalities provided a plausible competing explanation. The most balanced interpretation is high clinical suspicion for a neurological origin of the abdominal events, rather than confirmed abdominal epilepsy.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-2026-0009/rc

Peer Review File: Available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-2026-0009/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jeccm.amegroups.com/article/view/10.21037/jeccm-2026-0009/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the Declaration of Helsinki and its subsequent amendments. This report describes a single clinical case, involved no experimental intervention, and all clinical information was de-identified. Institutional ethics committee approval was not required for this single-patient case report according to local institutional requirements. Written informed consent was obtained from the patient for publication of this case report and any accompanying clinical information and the image. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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