The scenario describes a patient with a history of focal epilepsy, specifically temporal lobe epilepsy, who is being evaluated for potential epilepsy surgery. The patient has undergone extensive pre-surgical workup, including high-resolution MRI, ictal and interictal SPECT, and prolonged video-EEG monitoring. The MRI revealed a subtle hippocampal sclerosis, and the SPECT showed a hypoperfusion in the ipsilateral temporal lobe during the interictal period, with hyperperfusion during the ictal period. The video-EEG confirmed focal onset seizures originating from the anterior temporal lobe, with consistent semiology and scalp EEG findings. The question asks about the most appropriate next step in management to localize the seizure onset zone for potential resection. Given the concordant findings from multiple modalities pointing to the anterior temporal lobe, the most logical next step to refine the localization and assess the functional significance of this area is the implantation of intracranial electrodes. Specifically, stereo-EEG (SEEG) or subdural grid/strip electrodes would allow for direct recording of neuronal activity from the suspected epileptogenic region, providing higher spatial and temporal resolution than scalp EEG. This direct recording is crucial for differentiating between the irritative zone and the seizure onset zone, and for mapping eloquent cortex to avoid functional deficits during surgery. While other options might be considered in different contexts, they are less definitive for surgical planning in this specific, well-localized scenario. For instance, continuing with AEDs alone is unlikely to resolve the drug-resistant epilepsy. A repeat MRI might be considered if initial imaging was suboptimal, but here it revealed a lesion. A neuropsychological assessment is important for understanding cognitive deficits and potential post-surgical changes but does not directly localize the seizure onset zone. Therefore, invasive intracranial monitoring is the most appropriate step to precisely delineate the target for surgical intervention.

The core of this question lies in understanding the principles of pharmacokinetics and pharmacodynamics, specifically how drug metabolism affects therapeutic efficacy and potential toxicity in the context of epilepsy management. The scenario describes a patient with drug-resistant focal epilepsy who is being considered for adjunctive therapy with a new agent, levetiracetam. Levetiracetam is primarily renally excreted and does not undergo significant hepatic metabolism, making it a favorable option in patients with compromised liver function or those taking other medications that induce or inhibit hepatic enzymes. Conversely, carbamazepine, a common first-line AED, is extensively metabolized by the cytochrome P450 system, particularly CYP3A4, and is also an inducer of CYP1A2 and CYP2C19. This hepatic metabolism makes it susceptible to drug-drug interactions and can lead to variable serum concentrations, especially in patients with impaired hepatic function or those on other enzyme-inducing or inhibiting medications. The question asks to identify the most appropriate adjunctive antiepileptic drug (AED) for a patient with focal epilepsy who has a history of hepatic encephalopathy and is already on valproic acid. Valproic acid itself is primarily metabolized by glucuronidation and, to a lesser extent, CYP2C9 and CYP2C19, but its hepatic clearance is less affected by CYP induction compared to drugs like carbamazepine or phenytoin. However, the patient’s history of hepatic encephalopathy necessitates caution with AEDs that have significant hepatic metabolism or are known to exacerbate hepatic dysfunction. Considering the options: 1. **Phenytoin:** This AED is extensively metabolized by the liver via CYP2C9 and CYP2C19. It is also an inducer of CYP1A2, CYP2C9, CYP2C19, and CYP3A4. Its hepatic metabolism and enzyme-inducing properties make it a less ideal choice for a patient with a history of hepatic encephalopathy, as it could potentially worsen liver function or lead to complex drug interactions with valproic acid or other concurrent medications. 2. **Levetiracetam:** This AED is primarily excreted unchanged by the kidneys and undergoes minimal hepatic metabolism. It does not significantly induce or inhibit cytochrome P450 enzymes. This pharmacokinetic profile makes it a safer and more predictable option in patients with hepatic impairment or those on multiple medications, as it is less likely to cause drug-drug interactions or exacerbate liver issues. 3. **Ethosuximide:** This AED is primarily used for absence seizures and is metabolized by the liver, though to a lesser extent than phenytoin or carbamazepine. While generally well-tolerated, its primary indication is not focal epilepsy, and its hepatic metabolism still presents a consideration in a patient with hepatic encephalopathy. 4. **Vigabatrin:** This AED is primarily renally excreted and has minimal hepatic metabolism. It is a GABA transaminase inhibitor. While it has a favorable metabolic profile regarding the liver, its primary concern is visual field defects, which is a significant adverse effect that needs careful monitoring. However, in the context of hepatic encephalopathy, its renal excretion and lack of hepatic metabolism make it a viable consideration from a liver perspective. Comparing levetiracetam and vigabatrin, both have favorable hepatic profiles. However, levetiracetam has a broader spectrum of efficacy for focal epilepsies and a well-established safety profile in various patient populations, including those with comorbidities. Vigabatrin’s specific indication and significant visual side effect profile make levetiracetam a more generally preferred adjunctive therapy in this scenario, especially when considering the need for a new agent in drug-resistant focal epilepsy. The lack of hepatic metabolism and minimal CYP enzyme interactions for levetiracetam directly addresses the patient’s history of hepatic encephalopathy, making it the most prudent choice to minimize risks associated with liver dysfunction and drug interactions.

The core of this question lies in understanding the interplay between genetic predisposition, environmental triggers, and the resultant phenotype in epilepsy, specifically within the context of a developing brain. While many genetic epilepsies have known inheritance patterns, the penetrance and expressivity can be significantly modulated. In this scenario, the child presents with a complex partial seizure disorder and a history of febrile seizures, suggestive of an underlying predisposition. The identification of a de novo pathogenic variant in a gene known to be associated with early-onset epilepsy, particularly one affecting neuronal excitability or synaptic function, is crucial. The explanation for the observed phenotype requires considering not just the presence of the mutation but also its functional consequences. For instance, a mutation in a voltage-gated sodium channel gene could lead to hyperexcitability. The absence of a clear family history points towards a de novo event, a common occurrence in many severe genetic epilepsies. The explanation must then address why other options are less likely. Option b) is incorrect because while environmental factors are important, the presence of a confirmed pathogenic variant in a relevant gene provides a more direct and specific explanation for the epilepsy syndrome. Option c) is incorrect as it oversimplifies the genetic etiology, suggesting a single gene with complete penetrance and uniform expressivity, which is rarely the case in complex epilepsy syndromes. Option d) is incorrect because it focuses solely on a secondary insult without acknowledging the primary genetic vulnerability that likely underpins the susceptibility to such an insult and the subsequent development of epilepsy. The American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University emphasizes a comprehensive understanding of the multifaceted etiology of epilepsy, integrating genetic, environmental, and neurobiological factors.

The core of this question lies in understanding the differential diagnostic implications of specific EEG findings in the context of a patient with suspected non-epileptic seizures (NES), particularly differentiating them from focal epilepsy. The scenario describes a patient with a history suggestive of psychogenic non-epileptic seizures (PNES) who undergoes prolonged video-EEG monitoring. The critical finding is the absence of electrographic correlates during observed clinical events, coupled with the presence of generalized, brief, high-amplitude rhythmic delta activity (GHRDA) during periods of somnolence, which is a known artifactual phenomenon or a non-specific finding not indicative of epileptic activity. GHRDA, particularly when observed during drowsiness or sleep, is often associated with arousal from sleep or can be a manifestation of generalized slowing, but it does not represent a focal epileptic discharge. In contrast, focal epilepsy would typically manifest with focal interictal epileptiform discharges (e.g., spikes, sharp waves) originating from a specific brain region, or electrographic seizure activity that is spatially confined and evolves over time. The absence of such focal or generalized epileptiform discharges during the patient’s reported events strongly supports a diagnosis of NES. The explanation for why the other options are less likely is as follows: Focal slowing, while potentially present in epilepsy, is not the primary indicator of seizure activity and can be seen in various structural or metabolic brain abnormalities. The presence of brief, generalized rhythmic theta activity could be more suggestive of certain generalized seizure types, but the description of GHRDA in the context of somnolence points away from a true epileptic origin for the observed clinical events. Finally, the absence of any epileptiform discharges, even subtle ones, during the clinical events, combined with the artifactual nature of the GHRDA, makes a diagnosis of epilepsy unlikely in this specific presentation. Therefore, the most accurate conclusion based on the provided EEG findings and clinical events is the diagnosis of non-epileptic seizures.

The question assesses the understanding of the interplay between specific EEG findings and the underlying neurobiological mechanisms of epilepsy, particularly in the context of differentiating between focal and generalized epilepsies and their potential origins. The scenario describes a patient with a history suggestive of focal seizures, characterized by preserved awareness and focal motor symptoms. The EEG findings of intermittent rhythmic delta activity (IRDA) in the left temporal region, particularly during drowsiness, are crucial. IRDA, especially when localized and intermittent, can be a marker of underlying cortical dysfunction or irritation in the affected region. While IRDA can be seen in generalized slowing, its focal nature in this case points towards a localized epileptogenic zone. The absence of generalized spike-wave discharges or polyspikes argues against a primary generalized epilepsy. The presence of focal slowing, even if intermittent, in the temporal lobe, coupled with focal motor symptoms, strongly suggests a focal cortical origin, likely within the temporal lobe. This type of finding is highly relevant for pre-surgical evaluation at institutions like American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University, where precise localization is paramount. Understanding that focal slowing can represent an irritative zone or a consequence of underlying structural lesions is key. The explanation emphasizes that the temporal localization aligns with the semiology, and the intermittent nature of the IRDA, especially with drowsiness, is a common presentation of focal cortical dysfunction that can predispose to seizures. This differentiates it from generalized slowing seen in diffuse encephalopathies or the characteristic patterns of generalized epilepsies.

The core of this question lies in understanding the interplay between specific EEG findings and their implications for surgical candidacy in epilepsy, particularly in the context of a lesion identified on MRI. The scenario describes a patient with medically refractory focal epilepsy whose MRI reveals a subtle cortical dysplasia in the left temporal lobe. The EEG demonstrates intermittent rhythmic delta activity (IRDA) in the left temporal region, which is not directly concordant with the presumed seizure onset. IRDA is often associated with focal cortical dysfunction but can also be seen in non-epileptogenic lesions or even as a normal variant in certain sleep stages. Crucially, for surgical candidacy, the goal is to identify a region that is both the source of seizures and amenable to resection, with strong evidence of concordant interictal and ictal findings. The EEG showing IRDA in the left temporal region, while suggestive of some abnormality, does not provide definitive evidence of the epileptogenic zone. The absence of clear interictal epileptiform discharges (IEDs) or focal slowing directly correlating with the suspected seizure onset, and the lack of clear ictal discharges originating from the dysplasia, weakens the case for a straightforward surgical resection based on this single EEG. Video-EEG monitoring is the gold standard for localizing the seizure onset zone in refractory epilepsy. The current EEG, without the context of prolonged monitoring that captures habitual seizures, is insufficient to confirm the temporal lobe dysplasia as the sole or primary epileptogenic focus. Therefore, the most appropriate next step, as per established protocols for surgical evaluation at institutions like American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University, is to proceed with prolonged video-EEG monitoring. This will allow for the capture of habitual seizures, enabling precise localization of the seizure onset zone and assessment of its relationship to the MRI-identified lesion. This comprehensive approach is essential for determining if the patient is a suitable candidate for epilepsy surgery, ensuring that the proposed surgical target is indeed the source of the refractory epilepsy and that the resection will likely lead to seizure freedom with minimal neurological deficit. Other options, such as increasing AEDs without further localization, or proceeding directly to surgery based on a single, non-concordant EEG and MRI finding, would be premature and potentially lead to suboptimal outcomes or unnecessary interventions.

The question probes the understanding of the nuanced interpretation of EEG findings in the context of a patient with a history suggestive of focal epilepsy, specifically focusing on the significance of interictal epileptiform discharges in relation to a potential lesion. The scenario describes a patient with a history of focal impaired awareness seizures and a subtle T2-hyperintense lesion in the left temporal lobe on MRI. The EEG shows intermittent, brief, sharp waves maximal in the left temporal region during wakefulness, which are absent during sleep. The correct interpretation hinges on understanding that interictal discharges, particularly when localized to the vicinity of a suspected epileptogenic zone and absent during sleep, strongly support the lesion as the source of the epilepsy. This is because sleep can suppress or alter the expression of certain types of epileptiform activity, and the localization of discharges to the MRI-identified lesion is a key piece of evidence for surgical candidacy. The absence of generalized discharges or diffuse slowing further supports a focal etiology. Therefore, the most accurate conclusion is that the EEG findings are highly suggestive of the left temporal lesion being the epileptogenic focus.

The core of this question lies in understanding the interplay between specific seizure semiology, EEG findings, and the neuroanatomical localization that informs surgical candidacy for epilepsy. The patient presents with focal impaired awareness seizures characterized by auras of gustatory hallucinations and epigastric rising, followed by behavioral arrest and automatisms. This constellation of symptoms strongly suggests a temporal lobe origin, particularly the mesial temporal structures. The EEG findings of intermittent rhythmic delta activity in the left temporal region during the post-ictal phase, coupled with the absence of clear interictal epileptiform discharges in the routine EEG, necessitate further investigation to pinpoint the seizure onset zone. Video-EEG monitoring is crucial for correlating clinical events with electrical activity, and the identification of clear, consistent, and focal interictal spikes or rhythmic theta activity localized to the left anterior temporal region during these recordings would solidify the hypothesis of a left anterior temporal lobe epilepsy (LATE) focus. Functional neuroimaging, such as FDG-PET, is invaluable in demonstrating hypometabolism in the temporal lobe, often correlating with the seizure onset zone, especially in cases where MRI is subtle or normal. In this scenario, a left temporal hypometabolic region on FDG-PET that encompasses the anterior temporal lobe, particularly the amygdala and hippocampus, would strongly support surgical intervention. Therefore, the most appropriate next step, given the strong clinical suspicion and the need for precise localization for potential surgical resection, is to proceed with a comprehensive pre-surgical evaluation that includes detailed video-EEG monitoring and functional neuroimaging to confirm the suspected left anterior temporal focus. This systematic approach aligns with the rigorous standards of epilepsy surgery candidacy assessment at institutions like the American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University, emphasizing the integration of clinical, electrophysiological, and neuroimaging data for optimal patient management.

The scenario describes a patient with a history of focal epilepsy, specifically experiencing complex partial seizures originating from the left temporal lobe. The patient has undergone extensive pre-surgical evaluation, including high-resolution MRI revealing a subtle hippocampal sclerosis and stereo-EEG confirming the seizure onset zone. The goal is to select the most appropriate surgical intervention to achieve seizure freedom while minimizing neurological deficits, a core principle in epilepsy surgery at the American Board of Psychiatry and Neurology – Subspecialty in Epilepsy. The patient’s semiology (lip-smacking, automatisms, post-ictal confusion) and EEG findings strongly localize the seizure origin to the left temporal lobe, with the hippocampal sclerosis being the likely underlying pathology. For well-defined focal epilepsy with a clear, resectable lesion like hippocampal sclerosis, anterior temporal lobectomy with amygdalohippocampectomy is the gold standard. This procedure aims to remove the epileptogenic zone while preserving critical adjacent structures to prevent significant cognitive or memory deficits. Anterior temporal lobectomy involves removing the anterior portion of the temporal lobe, typically extending from the temporal pole posteriorly to the optic tract. Amygdalohippocampectomy specifically targets the amygdala and hippocampus, which are frequently involved in mesial temporal lobe epilepsy and are often the source of seizures in cases of hippocampal sclerosis. This combined approach offers a high likelihood of seizure control for this specific type of epilepsy. Other options are less suitable. Corpus callosotomy is primarily used for generalized epilepsy with disabling drop attacks and does not address focal seizure origins. Hemispherectomy is reserved for severe, intractable epilepsy affecting an entire hemisphere, usually due to extensive cortical dysplasia or stroke, and carries a higher risk of significant neurological deficits. Vagus nerve stimulation (VNS) is a neuromodulatory therapy used as an adjunct for drug-resistant epilepsy, not typically a first-line surgical option for a clearly defined focal lesion amenable to resection. Therefore, anterior temporal lobectomy with amygdalohippocampectomy is the most precise and effective surgical strategy for this patient’s condition, aligning with the advanced surgical principles taught and practiced at the American Board of Psychiatry and Neurology – Subspecialty in Epilepsy.

The core of this question lies in understanding the interplay between specific EEG findings and the likely underlying etiology of epilepsy, particularly in the context of a complex diagnostic challenge. The patient presents with focal impaired awareness seizures and interictal epileptiform discharges localized to the left temporal lobe. This localization is a critical piece of information. The presence of bilateral independent sharp waves, while initially confusing, needs to be interpreted in light of the overall clinical picture and the potential for secondary generalization or widespread network dysfunction. The key to differentiating between the options involves considering the typical EEG correlates of various epilepsy syndromes and etiologies. Option A is correct because the combination of focal temporal lobe seizures, left temporal interictal discharges, and the presence of a subtle hippocampal sclerosis on MRI strongly points towards mesial temporal lobe epilepsy (MTLE). MTLE is the most common cause of focal epilepsy in adults and is frequently associated with hippocampal sclerosis. The bilateral independent sharp waves, while not pathognomonic, can be seen in MTLE, potentially representing spread of abnormal activity or a more generalized network hyperexcitability that is not necessarily indicative of a distinct, separate epilepsy syndrome. The explanation for this option focuses on the high concordance between the clinical semiology, EEG localization, and neuroimaging findings, which is the gold standard for diagnosing MTLE. Option B is incorrect because while Lennox-Gastaut syndrome (LGS) is characterized by multiple seizure types, including tonic seizures and atypical absence seizures, and often shows a slow spike-wave pattern on EEG, the focal temporal lobe semiology and localized interictal discharges are less typical for LGS. LGS is generally considered a generalized epilepsy syndrome, and the EEG findings are usually more diffuse. Option C is incorrect because childhood absence epilepsy is primarily characterized by generalized spike-wave discharges on EEG, typically occurring in brief lapses of awareness. The focal semiology and localized temporal lobe findings in this patient are inconsistent with this diagnosis. Option D is incorrect because juvenile myoclonic epilepsy (JME) is characterized by generalized myoclonic jerks, often in the morning, and generalized polyspike-wave discharges on EEG. The focal impaired awareness seizures and localized temporal lobe EEG findings are not characteristic of JME. Therefore, the most parsimonious and diagnostically accurate interpretation of the presented findings, particularly the strong temporal lobe localization supported by both EEG and MRI, leads to the conclusion of mesial temporal lobe epilepsy.

The scenario describes a patient with drug-resistant focal epilepsy who is being evaluated for potential epilepsy surgery. The patient has undergone extensive pre-surgical workup, including high-resolution MRI, scalp EEG, and intracranial EEG (iEEG) monitoring. The iEEG data reveals consistent interictal epileptiform discharges (IEDs) localized to the left temporal lobe, specifically within the anterior hippocampus and parahippocampal gyrus. Furthermore, during iEEG monitoring, several habitual complex partial seizures were captured, originating from the same left temporal region. The patient’s neurological examination is otherwise unremarkable, and neuropsychological testing shows mild deficits in verbal memory, consistent with the suspected temporal lobe focus. The core principle in surgical candidacy for focal epilepsy is the identification of a well-defined, resectable epileptogenic zone that is responsible for the majority of disabling seizures, with minimal risk of significant neurological deficit post-resection. In this case, the convergence of iEEG findings (both interictal and ictal), MRI localization, and neuropsychological deficits strongly points to the left anterior temporal lobe, encompassing the hippocampus and parahippocampal gyrus, as the likely source of the epilepsy. Resection of this area, often termed a temporal lobectomy or selective amygdalohippocampectomy, is a well-established and effective surgical treatment for drug-resistant mesial temporal lobe epilepsy. The presence of consistent IEDs and captured habitual seizures originating from this specific region provides high confidence in its role in the epilepsy. The mild verbal memory deficits are also consistent with potential impairment in this region and suggest that while resection might impact memory, the benefits of seizure freedom often outweigh this risk, especially when the deficits are not profound. The other options are less appropriate. While a generalized epilepsy pattern would contraindicate focal resection, the iEEG clearly localizes the activity. Absence of clear MRI lesion does not preclude surgical candidacy, as many cases of mesial temporal lobe epilepsy have subtle or no visible MRI abnormalities. Furthermore, focusing on the right hemisphere would be incorrect given the clear left-sided localization of the epileptogenic zone. The question emphasizes the integration of multiple diagnostic modalities to pinpoint the source of the epilepsy, which is a cornerstone of pre-surgical evaluation at institutions like American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University.

The scenario describes a patient with drug-resistant focal epilepsy who has undergone extensive pre-surgical evaluation, including high-resolution MRI, scalp EEG, and intracranial EEG (iEEG). The iEEG data reveals consistent interictal epileptiform discharges (IEDs) localized to the left temporal lobe, specifically within the anterior hippocampus and parahippocampal gyrus. Furthermore, during a seizure captured on iEEG, the clinical semiology (lip-smacking, unresponsiveness, followed by a brief focal motor seizure in the right hand) correlates with the onset of rhythmic theta activity originating from the same left anterior temporal region. The goal is to identify the most appropriate next step in management, considering the goal of achieving seizure freedom while minimizing neurological deficits. The pre-surgical evaluation has successfully identified a concordant zone of epileptogenicity. The MRI has shown no gross structural lesion, suggesting a possible subtle cortical dysplasia or a mesial temporal sclerosis that might not be readily apparent on standard sequences. The scalp EEG, while showing some generalized slowing, did not precisely localize the seizure onset. The iEEG, however, provides high-resolution temporal and spatial data, pinpointing the origin to the left anterior hippocampus and parahippocampal gyrus. This mesial temporal localization is a common finding in drug-resistant epilepsy and is often amenable to surgical resection. Given the concordant findings from iEEG and clinical semiology, and the absence of a clear structural lesion on MRI that might suggest an alternative surgical target (like a tumor or vascular malformation), the most logical and evidence-based next step is to proceed with a tailored surgical intervention. Specifically, a selective amygdalohippocampectomy on the left side is indicated. This procedure targets the identified mesial temporal structures, which are the presumed generators of the seizures. The rationale is that removing or disabling this epileptogenic zone offers the highest probability of seizure control in this context. Other options are less appropriate. Continuing with further diagnostic iEEG without a clear plan for intervention would delay definitive treatment. Trying a different AED would be unlikely to succeed given the history of drug resistance and the clear localization of the seizure onset. A vagus nerve stimulator is a neuromodulatory therapy typically considered for patients who are not candidates for resective surgery or who continue to have seizures despite surgery, not as a first-line intervention after clear localization of a resectable focus. Therefore, proceeding with selective amygdalohippocampectomy is the most direct and effective approach to address the patient’s drug-resistant epilepsy based on the provided evaluation.

The scenario describes a patient with drug-resistant focal epilepsy who is being evaluated for surgical candidacy. The patient has undergone extensive pre-surgical workup, including high-resolution MRI, scalp EEG, and intracranial EEG (iEEG) monitoring. The iEEG data reveals consistent interictal epileptiform discharges (IEDs) localized to the left temporal lobe, specifically within the anterior hippocampus and parahippocampal gyrus. During the iEEG monitoring, spontaneous seizures were captured, originating from the same left anterior temporal region and spreading to adjacent mesial temporal structures before generalizing. The patient’s semiology is consistent with these findings, describing aura symptoms of rising epigastric sensation followed by focal impaired awareness seizures with automatisms. The core of the question lies in determining the most appropriate next step in management, considering the goal of achieving seizure freedom while minimizing neurological deficits. The pre-surgical evaluation has successfully identified a concordant zone of seizure onset. The presence of consistent IEDs and spontaneous seizures originating from the left anterior hippocampus and parahippocampal gyrus, coupled with concordant semiology, strongly suggests this region as the primary epileptogenic zone. Surgical resection of the identified epileptogenic zone is the most logical and evidence-based approach for drug-resistant focal epilepsy when a clear, localized source is identified. Specifically, a tailored anterior temporal lobectomy, potentially including the hippocampus and parahippocampal gyrus, is the standard surgical intervention for mesial temporal lobe epilepsy (MTLE) with clear localization. This approach aims to remove the tissue responsible for seizure generation. Considering the potential for cognitive deficits, particularly memory impairment, with left temporal lobe resections, a thorough neuropsychological assessment is crucial. However, the question asks for the *next* step in management *after* the comprehensive pre-surgical workup has identified the seizure focus. While neuropsychological assessment is part of the pre-surgical evaluation, the direct therapeutic intervention based on the confirmed localization is surgical resection. The other options represent less definitive or inappropriate management strategies in this context. Continuing to trial additional AEDs is unlikely to be effective given the documented drug resistance and clear localization of the seizure focus. Investigating for non-epileptic seizures (NES) is unwarranted as spontaneous seizures have been captured on iEEG, and the semiology is consistent with focal epilepsy. Recommending a vagus nerve stimulator (VNS) or responsive neurostimulation (RNS) would be considered if the patient were not a surgical candidate for resection due to the risk of significant neurological deficits or if resection failed to achieve seizure control. However, with a well-defined, resectable focus, direct surgical ablation is the preferred first-line surgical intervention. Therefore, proceeding with surgical resection of the identified left anterior temporal epileptogenic zone is the most appropriate next step.

The scenario describes a patient with a history of focal epilepsy, specifically experiencing complex partial seizures originating from the left temporal lobe. The patient has undergone a comprehensive pre-surgical evaluation, including high-resolution MRI revealing a hippocampal sclerosis, intracranial EEG demonstrating clear epileptiform discharges localized to the left anterior temporal region, and neuropsychological testing indicating mild deficits in verbal memory but preserved visual-spatial abilities. The goal is to determine the most appropriate next step in management, considering the established diagnosis, localization, and the patient’s functional status. The core principle guiding the decision is the effectiveness of resective surgery for medically intractable focal epilepsy with a clearly identified and localized epileptogenic zone. In this case, the left temporal lobe is implicated, and hippocampal sclerosis is a well-established cause of temporal lobe epilepsy amenable to surgery. Intracranial EEG provides definitive localization of the seizure onset, confirming the target for resection. The neuropsychological profile, while showing some deficits, does not contraindicate surgery, especially since the deficits are not in the hemisphere contralateral to the presumed surgical target (i.e., verbal memory deficits are expected with left temporal lobe surgery, and the patient’s visual-spatial abilities are preserved, suggesting the right hemisphere is relatively intact for those functions). Therefore, proceeding with a left anterior temporal lobectomy, including the hippocampus and amygdala, is the most evidence-based and logical step to achieve seizure freedom. This surgical approach directly addresses the identified source of the seizures. Other options, such as continuing with empirical trials of additional AEDs, are less likely to be effective given the presumed drug-resistant nature of the epilepsy and the clear surgical candidacy. Investigating alternative neuromodulation techniques would be premature without first attempting the most definitive treatment. Further diagnostic imaging without a clear indication for a different modality would also be an inefficient use of resources.

The core of this question lies in understanding the differential diagnostic process for paroxysmal neurological events, specifically distinguishing between epileptic seizures and psychogenic non-epileptic seizures (PNES) when EEG findings are equivocal or absent during an event. The scenario describes a patient with a history suggestive of epilepsy but without clear ictal EEG correlation during a witnessed event. The diagnostic approach in such a situation, particularly within the rigorous standards of the American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University, emphasizes objective evidence and systematic evaluation. The most definitive method for establishing a diagnosis when clinical suspicion for epilepsy remains high despite negative or inconclusive routine EEG is prolonged video-electroencephalographic (VEEG) monitoring. This technique allows for simultaneous recording of clinical events and corresponding EEG activity, providing the highest yield for capturing interictal epileptiform discharges or ictal patterns that confirm or refute an epileptic etiology. Furthermore, VEEG is crucial for observing behavioral manifestations that are characteristic of PNES, such as asynchronous eye closure, vocalizations not typically seen in epileptic seizures, or prolonged periods of immobility with preserved awareness. While other investigations like MRI are essential for identifying underlying structural lesions that can cause epilepsy, they do not directly confirm the presence of seizure activity. Neuropsychological testing can be valuable in assessing cognitive sequelae of epilepsy or characterizing functional neurological disorders, but it is not the primary diagnostic tool for differentiating seizure types in real-time. Genetic testing is becoming increasingly important for specific epilepsy syndromes but is not the immediate next step for diagnosing an ongoing paroxysmal event without clear EEG correlation. Therefore, the systematic capture and correlation of clinical events with EEG data via VEEG monitoring represents the most direct and evidence-based approach to resolving diagnostic uncertainty in this context, aligning with the advanced clinical assessment principles taught at the American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University.

The core of this question lies in understanding the neurophysiological basis of different seizure types and how they manifest on EEG, particularly in the context of a patient with a known history of focal epilepsy undergoing diagnostic evaluation. The scenario describes a patient with a history of left temporal lobe epilepsy who presents with episodes characterized by automatisms and impaired awareness, followed by a brief period of focal sensory aura. The EEG findings of rhythmic theta activity in the left temporal region, interspersed with brief bursts of sharp waves, are highly suggestive of a focal onset. Specifically, the presence of theta activity in the temporal lobe, especially when associated with behavioral changes like automatisms and impaired awareness, points towards a temporal lobe origin for the seizure. Sharp waves in the same region further localize the epileptogenic zone. While generalized spike-wave discharges would indicate a generalized epilepsy, and posterior slowing might suggest occipital or parietal involvement, the temporal findings are most consistent with the patient’s history and semiology. The absence of clear generalized discharges or other focal abnormalities makes the left temporal lobe the most probable site of origin for these events. Therefore, the EEG findings most strongly support a focal onset seizure originating from the left temporal lobe, aligning with the patient’s clinical presentation and known epilepsy syndrome.

The scenario describes a patient with drug-resistant focal epilepsy who has undergone extensive pre-surgical evaluation, including high-resolution MRI, scalp EEG, and intracranial EEG (iEEG). The iEEG data reveals consistent interictal epileptiform discharges (IEDs) localized to the left temporal lobe, specifically within the anterior hippocampus and adjacent parahippocampal gyrus. Furthermore, during spontaneous seizures captured on iEEG, the earliest ictal activity originates from this same region, with spread to the amygdala and then more widespread cortical involvement. The patient’s neurological examination is unremarkable, and neuropsychological testing shows mild deficits in verbal memory, consistent with left temporal lobe dysfunction. Given the concordant localization of IEDs and ictal onset zones, and the presence of a subtle mesial temporal sclerosis on MRI, the most appropriate next step in management, aligning with the principles of surgical evaluation for epilepsy at institutions like the American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University, is to proceed with a targeted resection of the identified epileptogenic zone. This approach aims to achieve seizure freedom by removing the brain tissue responsible for generating seizures. The other options are less appropriate at this stage. While continued medical management is an option for drug-resistant epilepsy, the clear localization of an epileptogenic zone makes surgical intervention a primary consideration. Investigating a potential non-epileptic seizure disorder would be less likely given the consistent iEEG findings of both IEDs and ictal onset. Introducing a novel AED without clear evidence of efficacy in this specific localization or seizure type would be premature and less targeted than surgical intervention.

The core of this question lies in understanding the differential diagnostic process for paroxysmal events in epilepsy, specifically differentiating between epileptic seizures and psychogenic non-epileptic seizures (PNES) when EEG findings are equivocal. The scenario describes a patient with a history suggestive of epilepsy but with interictal EEGs that are unremarkable and a witnessed event during a prolonged EEG recording that shows no clear epileptiform discharges, yet the patient reports subjective experiences consistent with their usual seizure aura. The crucial element is the absence of objective electrographic correlates during the event, which, in the context of a normal interictal EEG, raises suspicion for PNES. However, the patient’s consistent subjective aura, which is a focal neurological symptom, necessitates further investigation to rule out subtle or transient electrographic changes that might have been missed, or to consider focal cortical dysplasia or other subtle structural abnormalities not readily apparent on standard MRI. Therefore, the most appropriate next step, as per the rigorous diagnostic standards expected at the American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University, is to pursue a more comprehensive neurophysiological evaluation. This involves prolonged video-EEG monitoring, specifically designed to capture events and correlate them with detailed behavioral and subjective reports, and potentially advanced neuroimaging techniques that can detect subtle structural or functional abnormalities. While a trial of AEDs might be considered in some ambiguous cases, it is not the primary diagnostic step when the electrographic evidence is lacking and the possibility of PNES or a subtle focal seizure origin remains. Similarly, referral for psychological evaluation is important for PNES management but should follow a more definitive diagnosis. A thorough neurological examination is standard but unlikely to yield new definitive findings in this specific context if previous examinations were normal. The emphasis here is on refining the electrophysiological and neuroimaging assessment to achieve diagnostic certainty.

The scenario describes a patient with a history of focal epilepsy, specifically experiencing complex partial seizures originating from the left temporal lobe. The patient has undergone extensive pre-surgical evaluation, including prolonged video-EEG monitoring which localized the seizure onset to the mesial temporal structures, and high-resolution MRI revealing hippocampal sclerosis. The goal is to determine the most appropriate next step in management, considering the refractory nature of the epilepsy and the potential for surgical intervention. The patient’s epilepsy is refractory to multiple AEDs, a common indication for considering epilepsy surgery. The localization of seizure onset to the left temporal lobe, supported by both EEG and MRI findings, suggests a potential candidate for temporal lobectomy. However, before proceeding with a definitive ablative surgery, a crucial step involves assessing the patient’s functional lateralization, particularly concerning language and memory, to minimize the risk of significant post-operative deficits. The Wada test (intracarotid amobarbital procedure) is the gold standard for assessing hemispheric dominance for language and memory, especially in cases of left temporal lobe epilepsy where the dominant hemisphere is often involved. Performing the Wada test allows for the prediction of potential language deficits (aphasia) and memory impairment (amnesia) following a left temporal lobectomy. If the left hemisphere is found to be dominant for language and memory, and the right hemisphere cannot adequately compensate, then the risks of surgery must be carefully weighed against potential seizure relief. In such cases, alternative surgical approaches or continued medical management might be considered. Therefore, the most appropriate next step, given the established localization and refractory nature of the epilepsy, is to perform a Wada test to assess hemispheric functional lateralization before proceeding with a temporal lobectomy. This aligns with the principles of comprehensive pre-surgical evaluation at institutions like the American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University, emphasizing patient safety and maximizing functional outcomes.

The question assesses the understanding of the nuanced interpretation of EEG findings in the context of a patient with a history suggestive of focal epilepsy and a recent negative MRI. The core of the question lies in identifying the most appropriate next step in the diagnostic workup, considering the limitations of standard MRI and the potential for subtle epileptogenic lesions or non-lesional epilepsy. A standard MRI, while excellent for detecting gross structural abnormalities, may miss subtle cortical dysplasia, microgyria, or other architectural malformations that are not apparent on routine sequences. Furthermore, some epilepsies are purely functional or arise from networks without a clear structural correlate visible on conventional imaging. Therefore, a negative MRI does not definitively rule out focal epilepsy. Video-EEG monitoring is the gold standard for correlating clinical events with electrographic activity and localizing the seizure onset zone, especially when structural imaging is unrevealing or equivocal. It allows for detailed observation of semiology and simultaneous EEG recording, which is crucial for differentiating epileptic seizures from other paroxysmal events and for identifying the precise origin of seizures. Considering the patient’s history suggestive of focal epilepsy and the negative MRI, the next logical step to further investigate the potential focal origin and confirm the diagnosis is to proceed with prolonged video-EEG monitoring. This will provide objective evidence of seizure activity and help delineate the seizure onset zone, which is critical for guiding further management, including potential surgical evaluation. Other options are less appropriate at this stage. Repeating a standard MRI would likely yield similar results given the initial negative finding. A lumbar puncture is indicated for suspected CNS infections or inflammatory conditions, which are not suggested by the provided history. While genetic testing might be considered in specific epilepsy syndromes, it is not the primary next step for localizing a suspected focal onset in the absence of a clear syndromic diagnosis or a positive family history suggestive of a specific genetic etiology.

The core of this question lies in understanding the differential diagnostic process for paroxysmal neurological events, particularly distinguishing between epileptic seizures and psychogenic non-epileptic seizures (PNES) using prolonged video-EEG monitoring. A key indicator of PNES, especially in the context of a patient with a history of trauma and a lack of clear EEG ictal discharge, is the presence of specific semiological features that do not correlate with typical epileptic phenomena. These features often include prolonged episodes with waxing and waning intensity, complex motor behaviors that may appear purposeful or dramatic, and a lack of postictal confusion or alteration in consciousness. Furthermore, the absence of any epileptiform discharges on a prolonged EEG recording, despite the occurrence of events, strongly suggests a non-epileptic etiology. The explanation for why the other options are less likely involves considering the typical EEG and clinical presentations of focal or generalized epileptic seizures. Focal seizures, especially those originating from the temporal lobe, often have characteristic EEG changes and may present with automatisms, but the described semiology and lack of EEG correlate point away from this. Generalized seizures, while varied, typically involve bilateral EEG abnormalities and often a loss of consciousness or significant postictal impairment, which is not described here. The presence of auras, while suggestive of epilepsy, can also be mimicked by PNES, making it an insufficient sole criterion for diagnosis without supporting EEG findings. Therefore, the combination of specific semiological features and the absence of EEG correlation during events is the most compelling evidence for PNES.

The scenario describes a patient with a history of focal epilepsy, specifically experiencing focal aware seizures with secondary generalization. The patient has been on levetiracetam and lacosamide with suboptimal seizure control, indicating drug-resistant epilepsy. The question asks about the most appropriate next step in management, considering the American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University’s emphasis on comprehensive and evidence-based care. The patient’s seizure semiology (focal aware seizures with secondary generalization) and the failure of two first-line or commonly used second-line antiepileptic drugs (AEDs) strongly suggest the need for further investigation to identify a potential surgical target. Pre-surgical evaluation is a critical component of managing drug-resistant focal epilepsy, aiming to localize the epileptogenic zone. This evaluation typically involves advanced neuroimaging, prolonged video-EEG monitoring, and often neuropsychological testing. Considering the options: 1. **Increasing the dose of lacosamide or adding a third AED:** While a valid strategy in some cases, the patient has already failed two AEDs, and adding a third without further localization might not be the most efficient or effective next step, especially given the potential for polypharmacy and increased side effects. The focus at this stage should be on identifying the underlying cause of the drug resistance. 2. **Initiating vagus nerve stimulation (VNS):** VNS is a neuromodulation therapy often considered for generalized or focal epilepsies that are refractory to multiple AEDs, but it is typically considered after or in parallel with a thorough pre-surgical evaluation for focal epilepsy, as it does not aim to resect an epileptogenic focus. 3. **Performing a comprehensive pre-surgical evaluation:** This approach directly addresses the potential for surgical intervention, which offers the best chance for seizure freedom in select patients with drug-resistant focal epilepsy. It involves detailed investigations to precisely map the seizure onset zone and critical brain areas to avoid during resection. This aligns with the advanced diagnostic and therapeutic strategies emphasized in epilepsy subspecialty training. 4. **Recommending a ketogenic diet:** The ketogenic diet is a dietary therapy primarily used for pediatric epilepsy or certain specific genetic epilepsies, and while it can be effective in some adult cases of drug-resistant epilepsy, it is generally not the first-line approach for drug-resistant focal epilepsy in adults when surgical candidacy is a strong consideration. Therefore, the most appropriate next step, reflecting the comprehensive approach to drug-resistant focal epilepsy, is to proceed with a thorough pre-surgical evaluation to assess for surgical candidacy.

The scenario describes a patient with a history of focal epilepsy who is being evaluated for potential surgical intervention. The patient has undergone a comprehensive pre-surgical workup, including prolonged video-EEG monitoring and high-resolution MRI. The video-EEG identified a consistent pattern of interictal epileptiform discharges and several electrographic seizures originating from the left temporal lobe, correlating with subjective aura symptoms. The MRI revealed a small, T2-hyperintense lesion in the anterior hippocampus, consistent with hippocampal sclerosis. The goal is to determine the most appropriate next step in management, considering the evidence for a localized epileptogenic zone. The core principle guiding surgical candidacy in focal epilepsy is the identification of a well-defined, surgically amenable epileptogenic zone that, when resected, is likely to lead to seizure freedom without unacceptable neurological deficits. In this case, the concordant findings from both EEG and MRI strongly suggest a focal origin of the epilepsy in the left temporal lobe, specifically the hippocampus. The interictal and ictal EEG data pinpoint the likely source of the seizures, and the MRI lesion provides a potential anatomical substrate. Therefore, the most logical and evidence-based next step, as per established protocols for epilepsy surgery evaluation at institutions like American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University, is to proceed with a detailed surgical planning phase. This involves further localization techniques to precisely delineate the extent of the presumed epileptogenic zone and its relationship to critical functional areas. Techniques such as ictal SPECT, MEG, or even intracranial EEG (iEEG) might be considered depending on the clarity of the non-invasive findings and the specific surgical goals. However, given the strong concordance, proceeding directly to surgical planning for a temporal lobectomy, which is a well-established and effective procedure for mesial temporal lobe epilepsy, is the most appropriate course of action. This approach directly addresses the identified potential cause of the epilepsy with a proven therapeutic intervention.

The scenario describes a patient with drug-resistant focal epilepsy who is being evaluated for epilepsy surgery. The patient has undergone extensive pre-surgical workup, including high-resolution MRI, scalp EEG, and intracranial EEG (iEEG) monitoring. The iEEG data reveals consistent interictal epileptiform discharges (IEDs) localized to the left temporal lobe, specifically within the anterior hippocampus and parahippocampal gyrus. Furthermore, during the iEEG monitoring, the patient experienced several habitual focal impaired awareness seizures that were captured, with electrographic onset correlating precisely with the same left temporal lobe regions identified for IEDs. The neurological examination is otherwise unremarkable, and neuropsychological testing indicates mild deficits in verbal memory, consistent with the suspected temporal lobe focus. The core principle guiding surgical candidacy in such cases is the identification of a well-defined, resectable epileptogenic zone that is believed to be the primary source of the patient’s disabling seizures. The convergence of evidence from multiple modalities—structural neuroimaging (MRI), scalp EEG, and particularly the high-resolution localization provided by iEEG, which directly correlates with clinical seizure semiology—strongly supports a focal origin in the left temporal lobe. The hippocampus and parahippocampal gyrus are common sites for mesial temporal lobe epilepsy, a condition often amenable to surgical resection. Given the drug-resistant nature of the epilepsy and the clear localization of the presumed epileptogenic zone, surgical resection of the identified left temporal lobe structures, including the anterior hippocampus and parahippocampal gyrus, represents the most appropriate next step in management to potentially achieve seizure freedom. This approach aligns with the established evidence-based guidelines for surgical evaluation and treatment of drug-resistant focal epilepsy, aiming to improve quality of life by reducing or eliminating seizures.

The scenario describes a patient with drug-resistant focal epilepsy who has undergone extensive pre-surgical evaluation, including high-resolution MRI, scalp and intracranial EEG, and neuropsychological testing, all pointing to a unilateral temporal lobe focus. The question asks about the most appropriate next step in management, considering the goal of achieving seizure freedom while minimizing neurological deficits. The patient has failed multiple AED trials, indicating drug resistance. The comprehensive pre-surgical workup has localized the seizure onset to a specific brain region, making surgical intervention a viable option. The goal of epilepsy surgery is to resect the epileptogenic zone. Temporal lobectomy, specifically anterior temporal lobectomy with amygdalohippocampectomy, is the gold standard for mesial temporal lobe epilepsy, which is the most common type of focal epilepsy amenable to surgery. This procedure offers a high chance of seizure freedom with acceptable morbidity when performed in carefully selected patients. Considering the localization to the temporal lobe and the patient’s drug resistance, proceeding with surgical resection is the logical next step. Other options are less appropriate. Continuing to trial additional AEDs is unlikely to be effective given the documented drug resistance and the availability of a potentially curative surgical option. Investigating non-epileptic seizures is not indicated as the diagnostic workup has strongly supported an epileptic etiology. A vagus nerve stimulator or responsive neurostimulator are neuromodulation techniques typically considered for patients who are not candidates for resective surgery or who continue to have seizures despite resection, not as a first-line surgical intervention after clear localization. Therefore, the most appropriate next step is a temporal lobectomy.

The scenario describes a patient with a history of focal epilepsy originating in the left temporal lobe, who has undergone a successful anterior temporal lobectomy. Post-operatively, the patient exhibits a new pattern of generalized tonic-clonic seizures (GTCS) that are refractory to standard monotherapy with levetiracetam. The question probes the most appropriate next step in management, considering the patient’s surgical history and refractory GTCS. The core of the issue lies in understanding the potential causes of post-surgical GTCS and the principles of managing drug-resistant epilepsy in this specific context. The patient’s history of left temporal lobe epilepsy and subsequent surgery suggests a potential for altered network excitability or the development of new seizure onset patterns. The emergence of GTCS, particularly when refractory to an initial AED, necessitates a systematic approach. The first step in managing drug-resistant epilepsy, especially after a surgical intervention aimed at seizure control, is to optimize AED therapy. This involves considering alternative AEDs with different mechanisms of action and pharmacokinetic profiles. Given the refractory nature of the GTCS, switching to a broad-spectrum AED known for its efficacy in generalized epilepsies and its favorable tolerability profile is a logical progression. Levetiracetam, while effective for many seizure types, can sometimes be associated with paradoxical worsening of generalized seizures or the emergence of new seizure types in certain individuals. Therefore, a switch to an AED with a different primary mechanism, such as lacosamide, which modulates voltage-gated sodium channel slow inactivation, or brivaracetam, which has a higher affinity for synaptic vesicle protein 2A (SV2A) than levetiracetam and may offer a different efficacy profile, would be considered. However, the question asks for the *most* appropriate next step. Considering the options: 1. **Increasing the dose of levetiracetam:** While dose optimization is a standard step, the refractory nature of the GTCS and the potential for levetiracetam to exacerbate generalized seizures makes this less likely to be the most effective next step, especially if the current dose is already at a therapeutic level or approaching maximum. 2. **Adding a second AED:** Polytherapy is a common strategy for drug-resistant epilepsy. However, before adding a second agent, it is often prudent to ensure that the monotherapy has been maximally optimized or that a switch to a more appropriate monotherapy is considered, especially if the initial AED might be contributing to the problem. 3. **Switching to a different AED:** This is a strong contender. If the current AED is not effective or potentially contributing to the seizure pattern, a switch to an AED with a different mechanism of action and a proven track record in generalized epilepsies is a rational approach. 4. **Re-evaluating for non-epileptic seizures:** While always a consideration, the description of “generalized tonic-clonic seizures” suggests a clinical diagnosis of epilepsy, and the refractory nature points towards an epilepsy management issue rather than a primary diagnostic re-evaluation, unless there are specific clinical features suggesting otherwise, which are not detailed here. The most evidence-based and clinically sound next step for refractory GTCS, particularly in a post-surgical patient where the initial AED might not be optimal for the current seizure phenotype, is to switch to an AED with a different mechanism of action that has demonstrated efficacy in generalized epilepsies. Lacosamide is a well-established AED with a favorable profile for generalized tonic-clonic seizures and is often used in cases of drug resistance. Its mechanism of action, targeting sodium channel slow inactivation, differs significantly from levetiracetam’s SV2A binding. Therefore, switching to lacosamide represents a logical and evidence-based progression in management. The final answer is \(Lacosamide\).

The core of this question lies in understanding the differential diagnostic process for paroxysmal neurological events, specifically distinguishing between epileptic seizures and psychogenic non-epileptic seizures (PNES) using prolonged video-EEG monitoring. The scenario describes a patient with a history suggestive of both epilepsy and PNES, exhibiting complex motor phenomena and altered consciousness. The key to differentiating these conditions often lies in observing the electrographic correlates during the events. Epileptic seizures are characterized by abnormal, synchronized neuronal discharges that are typically visible on the EEG as epileptiform activity (e.g., spikes, sharp waves, spike-and-wave complexes) or specific ictal patterns. These patterns directly correspond to the observed semiology. Conversely, PNES, by definition, do not arise from abnormal cortical electrical activity and therefore will not show corresponding epileptiform discharges on the EEG during the events. While there might be non-specific EEG changes or artifacts, the absence of clear epileptiform activity during a clinically observed event strongly supports a diagnosis of PNES. The explanation for the correct option emphasizes this fundamental principle: the presence of clear, consistent epileptiform discharges on EEG during the observed events is the definitive electrophysiological marker of an epileptic seizure. Without such findings, even with convincing semiology, the diagnosis remains uncertain or leans towards non-epileptic phenomena. The other options are incorrect because they either misinterpret the significance of non-specific EEG changes, overemphasize subjective patient reports without electrographic correlation, or propose diagnostic criteria that are not universally accepted as definitive for distinguishing epileptic from non-epileptic events in the absence of clear EEG findings. The American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University places a high value on rigorous diagnostic methodology, which includes the critical interpretation of electrophysiological data in conjunction with clinical presentation.

The core of this question lies in understanding the differential diagnostic process for a patient presenting with paroxysmal neurological events, specifically distinguishing between epileptic seizures and psychogenic non-epileptic seizures (PNES). The provided EEG data, showing no epileptiform discharges during the observed events, is a critical piece of information. While a normal interictal EEG does not rule out epilepsy, the absence of any ictal abnormalities during documented episodes strongly shifts the suspicion towards non-epileptic phenomena. Furthermore, the patient’s history of significant psychosocial stressors, including recent job loss and marital discord, are well-established precipitants for PNES. The description of the events themselves, characterized by prolonged, waxing and waning motor activity with preserved consciousness and lack of post-ictal confusion, is also highly suggestive of PNES rather than focal or generalized epileptic seizures. Therefore, the most appropriate next step in management, given this clinical and electrophysiological picture, is to initiate a trial of cognitive behavioral therapy (CBT) specifically tailored for PNES. CBT addresses the underlying psychological factors contributing to the events and has demonstrated efficacy in reducing seizure frequency and improving quality of life in individuals with PNES. Other options are less appropriate at this stage. While further video-EEG monitoring could be considered if there remains significant diagnostic uncertainty, the current data strongly favors PNES. Antiepileptic drug (AED) monotherapy would be inappropriate and potentially harmful given the lack of evidence for epilepsy. Referral for neurosurgical evaluation is premature and unwarranted without a confirmed diagnosis of medically refractory epilepsy.

The core of this question lies in understanding the differential diagnostic process for paroxysmal neurological events, specifically distinguishing between epileptic seizures and psychogenic non-epileptic seizures (PNES). A key historical feature that strongly suggests PNES is the presence of prolonged, complex motor phenomenology that is inconsistent with typical epileptic seizure semiology, such as asynchronous limb movements, side-to-side head turning, or pelvic thrusting. Furthermore, the absence of postictal confusion or disorientation, coupled with a history of significant psychological trauma or stress, further supports a diagnosis of PNES. The electroencephalogram (EEG) findings are crucial; while an EEG during a typical epileptic seizure would demonstrate epileptiform discharges, the absence of such discharges during a witnessed event, especially when correlated with video monitoring, is highly indicative of a non-epileptic origin. The patient’s report of feeling “aware” during the event, though subjective, can also be a subtle clue, as awareness is often preserved in PNES, unlike many focal or generalized epileptic seizures. Therefore, the constellation of prolonged, complex motor activity without postictal deficits, normal interictal EEG, and a history suggestive of psychological distress points towards PNES as the most likely diagnosis.

The scenario describes a patient with drug-resistant focal epilepsy who is being evaluated for surgical candidacy. The patient has undergone extensive pre-surgical workup, including high-resolution MRI, scalp EEG, and intracranial EEG (iEEG) monitoring. The iEEG data reveals consistent interictal epileptiform discharges (IEDs) localized to the left temporal lobe, specifically within the mesial temporal structures. Furthermore, during iEEG, spontaneous seizures were captured, with the earliest propagating activity originating from the same left mesial temporal region. The patient’s clinical semiology, characterized by olfactory hallucinations followed by impaired awareness and automatisms, is also highly consistent with a left temporal lobe origin. Given this confluence of evidence – concordant localization from MRI, scalp EEG, iEEG IEDs, and seizure onset, coupled with a clinically suggestive semiology – the most appropriate next step in the management of this patient, aligning with the principles of epilepsy surgery evaluation at institutions like the American Board of Psychiatry and Neurology – Subspecialty in Epilepsy University, is to proceed with a targeted surgical resection of the identified epileptogenic zone. This approach aims to achieve seizure freedom by removing the brain tissue responsible for generating the seizures, while minimizing neurological deficits through precise localization and tailored surgical techniques. Other options, such as increasing AEDs, are less likely to be effective given the documented drug resistance and the clear localization of the epileptogenic zone. Continued iEEG monitoring without a clear plan for intervention would be a suboptimal use of resources. Investigating non-epileptic seizures is not supported by the strong localization data and concordant seizure semiology.