Diagnostic Overshadowing of Temporal Lobe Epilepsy: A Neuropsychiatric Blindspot in Young Adults

Abstract

Temporal Lobe Epilepsy (TLE) presents a unique diagnostic challenge due to its frequent clinical overlap with primary psychiatric disorders. In young adults, particularly those presenting with hallucinations, emotional dysregulation, and disordered eating, TLE may be mislabelled as psychosis or an affective illness, leading to delays in appropriate treatment and exposure to unnecessary pharmacological interventions. This paper explores the mechanisms by which TLE is overshadowed in psychiatric assessments, highlighting the significance of olfactory auras, automatisms, and post-ictal confusion as cardinal diagnostic features. We argue that standard EEG and emergency assessments are insufficient to exclude TLE in non-convulsive or atypical presentations, and that neuroimaging and prolonged telemetry are essential. Misdiagnosis can perpetuate neurological harm, psychiatric stigma, and inappropriate antipsychotic use, particularly in culturally diverse populations. Treatment with antiepileptic drugs such as sodium valproate has demonstrated efficacy in both seizure control and stabilisation of mood disturbances. Ultimately, the paper advocates for interdisciplinary approaches, neurologically-informed psychiatric screening, and enhanced clinical vigilance to mitigate diagnostic error and optimise outcomes for patients with focal epilepsies masquerading as psychiatric syndromes.

Introduction

Temporal Lobe Epilepsy (TLE), the most prevalent form of focal epilepsy, remains a clinically elusive condition when it manifests with psychiatric features that resemble primary mental health disorders. This is particularly problematic in young adults, where the emergence of hallucinations, behavioural change, and mood dysregulation frequently leads to early misclassification as psychosis, depression, or eating disorders. Despite significant advances in neuroimaging and electrophysiology, the diagnosis of TLE continues to be confounded by its psychiatric mimicry, compounded by systemic limitations in acute mental health services, and often perpetuated by diagnostic inertia.

The consequences of such misdiagnosis are substantial, not only does inappropriate treatment delay seizure control, but it may also expose patients to long-term iatrogenic risks, social stigma, and irreversible neurocognitive damage. In NHS acute mental health settings, such as during sectioning under the Mental Health Act 1983, time pressures and limited neurological access often lead to rapid psychiatric labelling. Up to 20–30% of TLE cases are initially misdiagnosed as psychiatric disorders (Clancy et al., 2014). Furthermore, the subtlety of non-convulsive seizure activity and the inherent limitations of routine EEGs highlight the need for epilepsy-sensitive screening approaches. This article critically examines the core clinical characteristics of TLE, elucidates the common pathways to misdiagnosis, and proposes evidence-based strategies for differential diagnosis and management. In doing so, it advocates for a neurologically informed, interdisciplinary model of care capable of mitigating diagnostic error and improving functional outcomes.

Diagnosis

TLE originates in the medial or lateral temporal lobes and often involves limbic structures such as the hippocampus and amygdala. Key diagnostic features include sensory auras, particularly olfactory hallucinations of burnt or metallic smells, déjà vu, gustatory illusions, and visceral sensations such as rising epigastric discomfort (Devinsky et al., 2018; Bartolomei et al., 2012). These often precede focal impaired-awareness seizures, which may involve automatisms such as lip-smacking, hand fumbling, or altered speech (Kanner, 2000). Post-ictal states frequently present with confusion, emotional volatility, paranoia, or transient memory disturbances, and may mimic psychosis or dissociative states (Trimble, 1991).

TLE diagnosis requires high-resolution magnetic resonance imaging (MRI) to assess for hippocampal sclerosis or other structural abnormalities (Jackson & Duncan, 1996). Electroencephalography (EEG) is essential, but interictal EEGs have a 40–50% false-negative rate (Hoare, 1984), particularly when seizures are infrequent or non-convulsive. Sleep-deprived or ambulatory EEG and video telemetry are often necessary to detect temporal lobe discharges (Lüders et al., 2006). Collateral history from relatives, carers, or community services is indispensable, particularly to identify subtle episodes, such as staring spells, behavioural arrest, or emotional lability, that patients may not recognise as seizures. Neurocognitive assessment may reveal memory deficits or executive dysfunction, further supporting a temporal origin.

Misdiagnosis

TLE is frequently mistaken for psychiatric illness, owing to its ability to mimic psychosis, affective instability, and behavioural dysregulation. Interictal psychosis and post-ictal confusion can involve hallucinations, persecutory ideation, and disorganised behaviour, prompting diagnoses such as schizophrenia or schizoaffective disorder (Mendez et al., 1993; Clancy et al., 2014). Similarly, autonomic seizures may provoke nausea or food aversion, leading to misdiagnosis as anorexia nervosa or depressive illness (Hill & Tennyson, 2003). The absence of generalised tonic-clonic seizures contributes to diagnostic ambiguity. In psychiatric settings, such non-convulsive or complex partial seizures are often misattributed to dissociation, catatonia, or psychogenic episodes (So et al., 1996).

On psychiatric wards, especially during emergency admissions, limited access to neuroimaging and EEG contributes to misdiagnosis. Rapid assessment protocols prioritise behavioural risk management over detailed neurological investigation. For instance, an EEG may not be ordered unless overt seizures are observed, and a normal result may falsely exclude epilepsy. Cultural factors further complicate diagnosis. In some communities, including those affected by mental health stigma, patients may hesitate to disclose “strange” experiences such as olfactory auras, fearing judgement or misunderstanding (Gureje et al., 2015). This may be interpreted as guarded or disorganised thinking, reinforcing psychiatric labels. Pharmacological suppression of TLE symptoms with antipsychotics can also obscure the clinical picture, creating a feedback loop in which the true aetiology remains concealed (Reuber, 2004).

Visual Aid 1: Table – Differential Diagnosis of TLE vs. Psychiatric Disorders

Purpose: To help clinicians distinguish TLE from common psychiatric disorders it mimics, addressing the misdiagnosis issue highlighted in the article.

Table Title: Differential Diagnostic Features of Temporal Lobe Epilepsy (TLE) vs. 

Primary Psychiatric Disorders.

Feature	Temporal Lobe Epilepsy (TLE)	Schizophrenia/Schizoaffective Disorder	Anorexia Nervosa	Major Depressive Disorder
Hallucinations	Olfactory  (e.g.,  burnt  smells),  gustatory,  or  visceral;  episodic  and  stereotyped	Auditory  (e.g.,  voices);  persistent,  non-stereotyped	Rare;  if  present,  related  to  starvation  (e.g.,  visual  distortions)	Rare;  if  present,  mood-congruent  (e.g.,  guilt-related)
Auras	Common  (e.g.,  déjà  vu,  epigastric  rising  sensation,  olfactory  hallucinations)	Absent	Absent	Absent
Behavioural Changes	Episodic  automatisms  (e.g.,  lip-smacking,  hand  fumbling);  post-ictal  confusion	Persistent  disorganized  behavior  or  negative  symptoms	Food  restriction,  body  image  distortion	Persistent  low  mood,  anhedonia
Memory Disturbances	Transient,  post-ictal  amnesia;  hippocampal-related  deficits	Working  memory  deficits;  not  episodic	Cognitive  slowing  due  to  malnutrition;  not  episodic	Concentration  difficulties;  not  episodic
EEG Findings	Temporal  lobe  discharges  (may  require  sleep-deprived  or  prolonged  EEG)	Normal  or  nonspecific  abnormalities	Normal	Normal
MRI Findings	Hippocampal  sclerosis,  temporal  lobe  lesions  (in  some  cases)	Normal  or  subtle  cortical  changes	Normal  or  cerebral  atrophy  (starvation-related)	Normal  or  nonspecific
Response  to Treatment	Improves  with  AEDs  (e.g.,  sodium  valproate);  antipsychotics  may  worsen  seizures	Improves  with  antipsychotics;  no  response  to  AEDs	Improves  with  nutritional  rehabilitation,  psychotherapy	Improves  with  antidepressants,  psychotherapy
Key Diagnostic Clue	Stereotyped,  episodic  symptoms  with  post-ictal  confusion	Chronic,  non-episodic  psychotic  symptoms	Body  image  distortion,  intentional  weight  loss	Persistent  mood  symptoms  without  episodic  neurological  features

Treatment

Early recognition and targeted treatment of TLE can reverse misdiagnosis and reduce the risk of iatrogenic harm. First-line antiepileptic drugs (AEDs) include sodium valproate (C₈H₁₅NaO₂), carbamazepine, and lamotrigine, with the choice guided by seizure type, psychiatric comorbidities, and individual tolerability (Devinsky et al., 2018; Engel, 2001). These agents not only stabilise neural excitability but often confer mood-stabilising properties, helping to alleviate interictal anxiety, irritability, or depressive symptoms (Kanner, 2006). Sodium valproate, in particular, is effective in managing focal seizures with mood dysregulation, though MHRA guidance mandates stringent pregnancy prevention protocols due to teratogenicity risk in women of childbearing age.

Risk of iatrogenic harm

The risk of iatrogenic harm in cases of misdiagnosed Temporal Lobe Epilepsy (TLE) is multifaceted and quite serious, especially when antipsychotics are prescribed for what is actually a neurological condition.

Pharmacological iatrogenesis: Antipsychotics like risperidone or olanzapine, often initiated when TLE is mistaken for psychosis, carry significant side effects, including weight gain, extrapyramidal symptoms, cognitive dulling, and metabolic syndrome. These not only impair quality of life but may also obscure the underlying seizure disorder by suppressing behavioural manifestations without addressing the epileptic activity itself.

Delayed seizure control: Failure to initiate antiepileptic drugs (AEDs) prolongs exposure to uncontrolled seizures, which increases the risk of neuronal injury (especially in mesial temporal structures like the hippocampus) and can worsen long-term cognitive outcomes. Chronic epileptiform activity has been linked to hippocampal atrophy and memory decline.

Psychosocial consequences: Being labelled with a primary psychiatric disorder, particularly a psychotic one, can lead to long-term stigma, inappropriate psychiatric hospitalisation, and limitations on autonomy (e.g., legal restrictions, employment exclusion), all of which may have been avoidable with earlier neurological identification.

Systemic entrenchment: Once a psychiatric diagnosis is coded into records, future clinicians may anchor to it, overlooking subsequent signs of epilepsy. This diagnostic inertia increases the likelihood of recurrent iatrogenic cycles.

Reproductive risk in women: Certain AEDs, like sodium valproate, though effective, carry teratogenic risks if not managed within MHRA guidelines. However, if the true diagnosis is delayed, these discussions and safeguards might not happen in time, especially if a patient is treated only under psychiatric protocols.

In drug-resistant cases, surgical evaluation is appropriate. Temporal lobectomy and stereotactic laser ablation offer seizure remission rates approaching 70–80%, particularly when MRI reveals mesial temporal sclerosis (Engel, 2001). Neuroimaging and neuropsychological testing guide surgical candidacy. Long-term care requires a biopsychosocial framework: seizure diaries, safety education, medication adherence support, and culturally sensitive psychoeducation. Empowering patients and families to recognise auras or post-ictal behaviours can improve diagnostic clarity and treatment engagement.

Crucially, interdisciplinary care is indispensable. Psychiatric and neurological teams must collaborate from the outset when psychiatric symptoms co-occur with atypical features such as olfactory hallucinations, transient amnesia, or episodic behavioural shifts. Services and cultural liaison officers can assist in history-gathering and reducing stigma. NHS systems should incorporate screening protocols for epilepsy in psychiatric settings, particularly when symptoms resist conventional treatment or show cyclical patterns suggestive of ictal states.

Conclusion

Temporal Lobe Epilepsy is one of the most clinically deceptive disorders in neuropsychiatry, with an alarming capacity for misdiagnosis as psychosis or affective illness. This diagnostic vulnerability is exacerbated by systemic pressures within psychiatric services, the subtlety of non-convulsive seizure activity, and the limitations of standard EEG and emergency mental health triage. The consequences of misdiagnosis, iatrogenic harm, loss of function, and delayed neurological care, are substantial.

To counter this, clinicians must maintain a high index of suspicion, particularly when evaluating young adults with episodic hallucinations, behavioural shifts, or uncharacteristic eating disturbances. Routine neurological screening, including EEG and MRI, should be considered in psychiatric settings for patients with atypical features. Furthermore, empowering patients and carers to report seizure equivalents, auras, or post-ictal confusion, reinforced by culturally competent psychoeducation, can help dismantle the barriers that delay accurate diagnosis. Ultimately, bridging the divide between psychiatric and neurological disciplines is not simply a theoretical goal but a clinical and ethical imperative.

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