Unusual case of topiramate-induced auditory-visual synaesthesia in a non-synaesthete young adult: a case report

Introduction

Background

Synaesthesia is a rare neurological condition in which stimulation of one sensory pathway involuntarily triggers an experience in another. While most individuals process sensory information through distinct, non-overlapping modalities, synesthetes may experience vivid cross-modal perceptions—such as tasting words, seeing sounds as colours, or attributing personalities to numbers (1). The phenomenon can be congenital or acquired, with the congenital form being relatively well-characterised in the literature and often considered a benign and enduring trait (2).

Acquired synaesthesia, by contrast, is less common and typically emerges later in life. Among the proposed aetiologies, pharmacologically induced synaesthesia represents a particularly rare subtype. This occurs when certain substances or medications—especially those that alter neurochemical pathways—trigger novel cross-sensory experiences (3). Anecdotal reports have implicated psychoactive agents such as lysergic acid diethylamide (LSD) and psilocybin, but there remains a scarcity of formal documentation regarding synaesthesia precipitated by prescription medications (4,5).

Topiramate is a medication used widely in the management of epilepsy and for migraine prophylaxis. Its mechanisms of action include sodium channel blockade, potentiation of GABAergic (gamma-aminobutyric acid) transmission, inhibition of excitatory glutamate receptors, and carbonic anhydrase inhibition (6). These actions affect neuronal excitability and may influence sensory integration at the cortical level. Although topiramate is associated with a variety of cognitive and perceptual side effects, reports of it inducing synaesthesia are exceptionally rare (7).

Rationale and knowledge gap

Pharmacologically induced synaesthesia remains poorly recognised in clinical practice, especially in primary care, where initial medication histories are often taken and side effects first emerge (1,3,7). The rarity of these presentations, coupled with the absence of clear diagnostic criteria, makes identification and reporting challenging. In particular, topiramate-induced synaesthesia is underreported in the literature, and its pathophysiology is not well understood (3-5). Most published cases focus on recreational drug-induced experiences or congenital forms, leaving a significant gap in our understanding of drug-induced perceptual alterations arising from commonly prescribed neurological medications.

There is growing interest in the neuropharmacological mechanisms that could underpin these experiences (6,7). It is hypothesised that medications like topiramate may either mimic or unmask latent synaesthetic connections by modulating cortical excitability or disinhibiting cross-modal sensory pathways. However, very few case studies have systematically documented this, especially from a diagnostic and therapeutic perspective in general practice.

Objective

This case report aims to describe an unusual case of auditory-visual synaesthesia in a young adult following the initiation of topiramate for migraine prophylaxis. It provides a comprehensive diagnostic workup, discusses potential mechanisms, and reflects on the role of primary care clinicians in identifying, managing, and reporting such rare adverse drug reactions. By doing so, it contributes to the limited but growing body of literature on acquired drug-induced synaesthesia and calls for increased clinical awareness and patient dialogue regarding uncommon perceptual side effects. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-103/rc).

Case presentation

A 28-year-old male software engineer with no prior significant medical or psychiatric history presented to their general practitioner (GP), reporting unusual and unexpected sensory experiences. Approximately two weeks after initiating topiramate for migraine prophylaxis, the patient began to experience involuntary, vivid visual perceptions triggered by specific auditory stimuli. Notably, these included seeing green swirls upon hearing a mobile phone ring and perceiving purple hues when hearing rainfall. These cross-sensory experiences—hallmarks of auditory-visual synaesthesia—were consistent, specific, and repeatable.

The auditory-visual synaesthetic experience was identified and tracked using structured clinical interviews across multiple visits. Although the patient described specific, consistent, and repeatable perceptual phenomena, no formal psychophysical or neurocognitive tests were conducted due to the self-limited nature of symptoms and the clear temporal relationship with topiramate initiation. The patient reported no accompanying distress but described the phenomenon as curious and disorienting enough to seek medical advice.

The experiences occurred multiple times daily, often triggered by specific environmental sounds such as mobile phone rings, music, or rainfall. Each episode lasted several seconds to a few minutes and was described as vivid but non-intrusive. For example, the patient saw swirling green patterns with phone rings and diffuse purple hues during rainfall. He consistently reported that the colours were spatially located in his visual field, not imagined, and occurred automatically without conscious effort.

A comprehensive medical history and physical examination were conducted during the initial consultation. The patient had no history of recreational drug use, alcohol misuse, neurological illness, or mental health conditions. There was no family history suggestive of synaesthesia or neurological disease. The patient’s lifestyle and daily routines had remained unchanged, reducing the likelihood of psychosocial triggers. Both physical and neurological examinations, including visual and auditory assessments, were unremarkable with no signs of infection, inflammation, or focal deficits.

Topiramate, recently initiated for migraine prophylaxis, was the only new medication identified during the review. No other pharmaceutical, herbal, or over-the-counter treatments had been added or changed. The GP suspected a potential pharmacological cause, given the strong temporal association between the initiation of topiramate and the onset of synaesthetic experiences. A provisional diagnosis of drug-induced synaesthesia was made, and the patient was referred to neurology for further assessment.

A multidisciplinary diagnostic workup was initiated. Magnetic resonance imaging (MRI) of the brain was performed using T1 and T2-weighted sequences, revealing no structural abnormalities, lesions, or tumours. Audiological evaluation—including pure tone audiometry, speech recognition thresholds, and otoacoustic emissions—yielded results within normal limits, excluding auditory pathology. Ophthalmological assessment involved a full visual field test, fundoscopic examination, and optical coherence tomography (OCT), all of which showed normal findings. The absence of sensory deficits or structural changes in both the visual and auditory systems strengthened the likelihood of a functional, drug-induced process.

Given the exclusion of alternative causes and the confirmed timing of symptom onset in relation to topiramate initiation, the diagnosis of pharmacologically induced synaesthesia was supported. A shared decision was made between the GP and the patient to discontinue topiramate. The patient was closely monitored throughout this period to detect any adverse effects of withdrawal and to assess symptom resolution.

Following cessation, a structured follow-up schedule was established with reviews at one week, two weeks, four weeks, and then monthly for three months. During these consultations, clinicians evaluated both migraine control and the persistence or resolution of synaesthetic symptoms (Table 1). A gradual reduction in perceptual alterations was noted over the first month, with complete resolution reported by the end of the second month. No recurrence of synaesthetic experiences was observed thereafter. Symptom resolution was similarly monitored qualitatively during scheduled follow-ups through direct patient interviews.

For ongoing migraine prophylaxis, the patient was offered and agreed to start propranolol, chosen for its efficacy and lower likelihood of neuropsychiatric side effects. The patient tolerated propranolol well and reported good control of migraine frequency and intensity without any new or unusual sensory experiences. At the three-month follow-up, the patient expressed satisfaction with the management plan, highlighting both relief from migraines and the resolution of the unsettling synaesthetic symptoms.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Key findings

This case report presents a rare and clinically significant instance of drug-induced synaesthesia in a young adult following the initiation of topiramate for migraine prophylaxis. While synaesthesia is classically considered a congenital condition, this case exemplifies how it can also emerge abruptly in response to pharmacological agents. The patient’s presentation was characterised by consistent auditory-visual experiences, triggered by routine environmental sounds, and occurring without any prior history of neurological or psychiatric illness. The synaesthetic symptoms resolved gradually after the withdrawal of topiramate, confirming a likely causal relationship.

To our knowledge, this is one of very few documented cases of topiramate-induced synaesthesia in the medical literature. The temporal correlation between medication initiation and symptom onset, combined with a comprehensive exclusion of structural or primary sensory pathologies, supports the diagnosis of pharmacologically induced perceptual alteration. This case also underscores the value of primary care in recognising and managing unusual neurological side effects through structured follow-up and collaborative decision-making.

Strengths and limitations

This case’s primary strength lies in the detailed diagnostic process, which included clinical examination, neuroimaging, audiological testing, and ophthalmological evaluation. It also demonstrates the importance of a systematic approach in excluding differential diagnoses and arriving at a diagnosis of exclusion. Furthermore, the resolution of symptoms post-medication withdrawal strengthens the clinical inference.

However, as a single-patient report, its generalisability is limited. The transient nature of pharmacologically induced synaesthesia also restricts the opportunity for extended observational study. Additionally, the diagnosis relies heavily on the patient’s self-reported experiences, which, while consistent and credible, remain inherently subjective.

Comparison with similar research

Existing literature on drug-induced synaesthesia is largely anecdotal and often focuses on psychedelic or recreational substances. Psychoactive agents such as LSD, psilocybin, and 2C-B have been shown to produce transient synaesthetic experiences in non-synesthetes (1,2,7,8). In contrast, reports of similar effects caused by clinically prescribed medications are rare. Topiramate’s primary use is not psychoactive but anticonvulsant and prophylactic, making this case particularly notable (9,10).

Previous studies have explored the neurological underpinnings of congenital synaesthesia, pointing to cross-activation of adjacent sensory cortices and reduced sensory inhibition (3,4,11,12). The mechanisms by which topiramate might replicate or induce similar cortical interactions are speculative but align with theories of altered GABAergic and glutamatergic signalling contributing to perceptual integration anomalies (5,6).

Explanations of findings

Topiramate’s pharmacological profile includes enhancement of GABAergic activity, inhibition of glutamate receptors, and sodium channel blockade (7,13-15). These neurochemical effects modulate cortical excitability and may result in the disinhibition or cross-activation of sensory networks—proposed mechanisms underlying synaesthesia.

The abrupt onset of symptoms in a previously asymptomatic individual suggests an acquired phenomenon rather than the unmasking of congenital synaesthesia. Furthermore, the consistent nature of the experiences and their resolution following topiramate discontinuation reinforce a drug-induced origin. Normal imaging and sensory testing excluded other potential aetiologies, such as migraine aura, hallucinations, or structural abnormalities (1,2,6,14).

The differential diagnosis included hallucinatory phenomena and migraine-associated perceptual disturbances (Table 2). However, unlike migraine aura, the synaesthetic responses were repeatable, specific to individual auditory cues, and not associated with headache onset (3,5,12,14). This distinction highlights the importance of detailed history-taking and understanding patient-reported experiences in evaluating perceptual symptoms.

This case demonstrates the capacity of a widely prescribed medication to trigger complex perceptual alterations, reinforcing the need to consider even uncommon side effects during clinical review. It also illustrates how perceptual symptoms, though benign, may be alarming to patients and require clear explanation and reassurance.

It is noteworthy that synaesthesia is not listed as an adverse effect in the current summary of product characteristics for topiramate, underscoring the importance of case reports in identifying rare but clinically meaningful neuropsychiatric effects.

Implications and actions needed

This case highlights the need for greater clinical awareness of rare but impactful adverse drug reactions. In primary care, where medication initiation and follow-up commonly occur, clinicians should maintain an open and non-dismissive approach to patients describing unusual perceptual changes. Early identification and appropriate escalation can prevent unnecessary anxiety and facilitate alternative treatment strategies.

The case also supports a multidisciplinary approach to symptom evaluation, including neurological, audiological, and ophthalmological assessments where indicated. Medication histories should be revisited systematically when new neurological or sensory symptoms arise. This is especially relevant in the context of neurological medications like topiramate, which have wide-ranging effects on brain function.

Finally, the case contributes to the growing understanding of synaesthesia and underscores the need for further clinical and neuroscientific research into pharmacologically induced variants. Awareness, reporting, and investigation of such rare presentations can enhance patient safety and deepen insights into brain–mind relationships.

Conclusions

This case highlights a rare instance of topiramate-induced auditory-visual synaesthesia in an otherwise healthy young adult, underscoring the importance of awareness among primary care providers regarding uncommon medication-related neuropsychiatric symptoms. Prompt identification, detailed medication history, and collaborative multidisciplinary evaluation are essential in managing atypical perceptual changes. This report contributes to the limited but growing literature on pharmacologically induced synaesthesia, advocating for increased clinical vigilance and further research into medication-induced cross-modal sensory phenomena.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-103/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-103/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-103/coif). W.J. serves as an unpaid editorial board member of AME Case Reports from July 2024 to June 2026. The other 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 ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report. 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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