Acute Symptomatic Seizure Triggered by Eucalyptus Exposure in a Young Adult: A Case Report

Abstract

Eucalyptus oil is a commonly used over-the-counter herbal preparation for the management of minor respiratory ailments and is widely perceived as safe. However, its principal constituent, 1,8-cineole, has been associated with neurotoxic and seizurogenic effects. We report the case of a 20-year-old male with no prior history of epilepsy who presented to the emergency department following an unwitnessed nocturnal seizure characterized by tongue bite, postictal confusion, and autonomic symptoms. The episode occurred after recent consumption of eucalyptus oil for upper respiratory tract infection. On evaluation, the patient was conscious and oriented with no focal neurological deficits. Laboratory investigations, including serum electrolytes and metabolic parameters, were within normal limits, while inflammatory markers were mildly elevated. Magnetic resonance imaging of the brain with epilepsy protocol and serial electroencephalograms revealed no epileptiform abnormalities. The temporal relationship between eucalyptus oil exposure and seizure onset, along with the absence of recurrent seizures following discontinuation of the oil, supported the diagnosis of an acute symptomatic seizure rather than epilepsy. Management included short-term antiepileptic therapy, withdrawal of the offending agent, and supportive care without the need for long-term antiepileptic medication. Clinical pharmacist involvement through detailed medication reconciliation, identification of eucalyptus oil as a probable trigger, and patient counselling played a key role in preventing recurrence. This case emphasizes the importance of clinician awareness and careful history taking regarding herbal and over-the-counter product use in patients presenting with first-episode seizures.

Keywords

Introduction

Since ancient times, it is a common practice to treat minor illnesses like common cold, sinus congestion with essential oils like Eucalyptus oil. Eucalyptus oil is the distilled volatile aromatic constituent extracted from the leaves of Eucalyptus, a genus of the plant family Myrtaceae. It is available easily as over the counter medication in the form of cough drops, ointments, balms and mouthwashes. It can be administered by mouth, through the nose, or applied to the skin ⁽¹⁾.

Eucalyptus oils are complex blends of volatile organic compounds, with monoterpenes forming the major group of constituents. In pharmaceutical-grade eucalyptus oil, the key active component is 1,8-cineole (eucalyptol), which is required to make up at least 70% of the oil. Among the different species, Eucalyptus kochii and Eucalyptus polybractea contain the highest levels of cineole, typically ranging between 80% and 95%. On a global scale, Eucalyptus globulus is the primary source used for commercial production. It is important to note that the final chemical composition of eucalyptus oil may vary depending on how the raw plant material is stored and the extraction method used⁽²⁾.

Mechanism:

Experimental animal models suggest that the proposed pathophysiological mechanism involves increased neuronal hyperexcitability. This effect is thought to occur due to protein kinase A–mediated inhibition of potassium ion channels, leading to disruption of the sodium–potassium gradient across the cell membrane⁽³⁾.

CASE REPORT

A 20 year old male patient was presented to the emergency department following an unwitnessed episode during sleep which he does not recall with no available bystander. He reported waking up with profuse sweating, blood mixed with saliva on his pillow, bruises over his fingers, and blood stains in the washroom, and examination revealed a tongue bite. The patient’s past medical history revealed childhood asthma, diagnosed at the age of 8–9 years, for which he received pharmacological treatment for approximately two years, later discontinued . He also had a history of low grade fever, sore throat, cold and cough for the past 3-4 days, for which he had consumed two tablespoons of Eucalyptus oil which could be probable cause of seizures. His past medication history includes tablet Fexofenadine 120 mg orally once daily and tablet Paracetamol 650mg orally twice daily. On arrival to the ER, the patient was conscious, oriented and obeying commands, with no focal neurological deficits. In view of a suspected seizure, he was administered intravenous Levetiracetam 1gm stat. Initial EEG showed no epileptiform discharges, and MRI brain with epilepsy protocol was normal. His metabolic parameters were within normal limits. Chest X-ray was normal. Inflammatory markers showed a C-reactive protein (CRP) level of 13 mg/L and a total leukocyte count of 10,000 cells/mm³. Serum electrolytes revealed sodium of 142 mmol/L and potassium of 4.1 mmol/L. Serum IgE level was elevated at 396 IU/mL. He was started on   antibiotics(Cefoperazone&Sulbactum and Doxycycline), bronchodilator nebulizations Formoterol Fumarate & Budesonide and antihistamines Montelukast & Levocetirizine. A repeat bedside EEG was performed after 24 hours which showed no discharges. Flu panel was negative. Antibiotics were stopped. As he had no further episodes of seizures he was planned for discharge with advice to continue Montelukast–Levocetirizine, inhaled Formoterol Fumarate–Budesonide, Azelastine Hydrochloride–Fluticasone nasal spray, and Aceclofenac–Paracetamol was prescribed for pain  and advised to follow up in the OPD after 5 days.

DISCUSSION

Eucalyptus oil (EO) is a commonly used over-the-counter herbal preparation for symptomatic relief of upper respiratory tract infections. Despite its widespread perception as a safe and natural remedy, increasing evidence suggests that EO possesses significant neurotoxic and seizurogenic potential, particularly due to its major constituent, 1,8-cineole (eucalyptol). This case highlights an acute symptomatic seizure temporally associated with recent EO exposure in a previously healthy young adult, emphasizing the need for heightened clinical awareness.

Several case reports and observational studies have documented seizures following ingestion, inhalation, or topical application of eucalyptus oil, even at therapeutic or seemingly innocuous doses. Both pediatric and adult populations have been affected, with seizures often occurring within minutes to hours of exposure. In many cases, patients had no prior history of epilepsy, similar to the present case, supporting the role of EO as a direct precipitating factor rather than an unmasking of an underlying epileptic disorder^(4,5).

The proposed mechanism underlying EO-induced seizures involves neuronal hyperexcitability mediated by 1,8-cineole. Experimental studies have demonstrated that eucalyptol inhibits potassium ion channels via protein kinase A–dependent pathways, resulting in prolonged neuronal depolarization and increased action potential firing. This disruption of the sodium–potassium gradient enhances cortical excitability and lowers the seizure threshold. Additionally, monoterpenes present in EO are highly lipophilic, enabling rapid penetration across the blood–brain barrier and facilitating central nervous system toxicity ⁽⁶⁾.

In the present case, the patient had an antecedent upper respiratory tract infection and elevated inflammatory markers, which may have further contributed to a transient reduction in seizure threshold. Fever, systemic inflammation, and sleep deprivation are recognized as seizure-precipitating factors and may act synergistically with neurotoxic agents such as EO. Although the patient also had a history of childhood asthma and elevated serum IgE levels, there is no strong evidence linking atopy itself to seizure occurrence, suggesting that EO exposure was the most plausible trigger.

Neuroimaging and electroencephalographic findings in EO-related seizures are frequently normal, as observed in this patient. The absence of epileptiform discharges on serial EEGs and the lack of recurrent seizures after discontinuation of EO strongly support the diagnosis of an acute symptomatic seizure rather than epilepsy. This distinction is clinically important, as long-term antiseizure medication may not be required once the offending agent is avoided^(4,7).

This case underscores the importance of obtaining a detailed history of complementary and alternative medicine use in patients presenting with first-episode seizures. Given the easy availability of EO and lack of public awareness regarding its potential neurotoxicity, clinicians should actively counsel patients on its risks. Regulatory labelling and public health education may help reduce preventable EO-related neurological adverse events.

CONCLUSION

This case highlights eucalyptus oil as a potential and often overlooked cause of acute symptomatic seizures, even in individuals without a prior history of epilepsy. The temporal association between eucalyptus oil exposure and seizure onset, along with normal neuroimaging and electroencephalographic findings and the absence of seizure recurrence after discontinuation, strongly supports its role as the precipitating factor in this patient. Given the widespread availability and common use of eucalyptus oil for minor respiratory ailments, clinicians should maintain a high index of suspicion for essential oil–induced neurotoxicity in patients presenting with first-episode seizures. Careful history taking regarding the use of over-the-counter and herbal preparations is essential to avoid misdiagnosis and unnecessary long-term antiseizure therapy. Increased public awareness and appropriate counselling regarding the potential neurological risks of eucalyptus oil may help prevent similar adverse events.

ROLE OF PHARMACIST

A detailed medication and over-the-counter product history was carefully taken, through which the use of eucalyptus oil was recognized as a possible trigger for the seizure. The patient’s existing medications were thoughtfully reviewed to rule out other drug-related causes and to avoid unnecessary long-term antiepileptic treatment. Clear counselling was provided about the potential risks of essential oils, and guidance on safe medication practices was given to help prevent recurrence.

CHALLENGES

Diagnosing eucalyptus oil–induced seizures can be difficult because many patients do not consider herbal products as medications and may not mention their use unless specifically asked. Since routine tests such as MRI and EEG are often normal, it becomes challenging to differentiate this condition from new-onset epilepsy. The presence of fever or respiratory infection can further confuse the clinical picture. Limited awareness among healthcare professionals about the seizurogenic potential of essential oils may lead to misdiagnosis and unnecessary long-term antiepileptic therapy. Treatment mainly involves stopping the offending agent and supportive care, but deciding the duration of therapy can be uncertain in the absence of clear guidelines.

REFERENCES

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