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Introduction The established diagnostic method attempts to produce a unifying diagnosis explaining all of a patient‘s symptoms. In many patients with neuropsychiatric disease however there are multiple coexistent pathologies, making the process of ascribing symptoms to discrete diagnoses difficult. We describe the case of a patient eventually diagnosed with temporal lobe epilepsy and frontotemporal dementia.Case Presentation A 70-year-old man presented with cognitive impairment and a tonic-clonic seizure. He had a background of childhood epilepsy, stopping antiepileptics in his early teens and remaining seizure-free until presentation. His wife reported losses of autobiographical memory, progressive apathy and aphasia. On cognitive assessment there were naming errors/anomia and reduced verbal fluency. On subsequent assessments increasingly frequent unresponsive episodes concerning for subclinical seizures were reported, despite escalating antiepileptic treatment.Serial MRI head scans demonstrated a left amygdala and medial temporal lobe enlargement with T2 hyperintensity but no contrast enhancement. Autoantibody panels demonstrated a modestly raised anti-GAD but were otherwise negative. A trial of immunosuppression for possible autoimmune encephalitis led to neither radiological nor clinical improvement, with worsening behavioural changes and speech.Ambulatory EEG demonstrated subclinical epileptic focal seizures in the left medial temporal area spreading to the left frontal lobe with interictal abnormalities in the left medial temporal area. Further escalation of antiepileptic therapy led to resolution of the patient‘s unresponsive episodes and normalisation of the EEG. A repeat MRI demonstrated resolution of the amygdala asymmetry but progressive cortical atrophy. Despite treatment of the epilepsy the patient continued to deteriorate cognitively. A diagnosis of behavioural variant frontotemporal dementia was made.Discussion Temporal lobe epilepsy is associated with a range of neuropsychiatric symptoms, complicating the diagnosis of coexistent neuropsychiatric disease. It was only on adequate treatment of the seizures and elimination of temporal lobe epilepsy from the differential diagnosis that frontotemporal dementia was diagnosed. While amygdala pathology is associated with frontotemporal dementia, this generally refers to atrophy rather than enlargement. Amygdala enlargement has been suggested as a distinct subtype of temporal lobe epilepsy, although some have argued that this represents a secondary process in reaction to frequent temporal lobe seizures rather than a primary pathology. A reactive process would explain the resolution of the amygdala asymmetry in this case following epilepsy treatment.Conclusion This case highlights that clinicians should be vigilant to the possibility of alternate diagnoses when behavioural symptoms do not resolve with treatment of epilepsy. Frontotemporal dementia can mimic the neuropsychiatric comorbidities of epilepsy, complicating the diagnosis of both conditions.