Lamotrigine Treatment Research Articles

Rash and Liver Dysfunction Related to Lamotrigine Therapy

Objective: To report a case of rash and liver dysfunction associated with lamotrigine treatment. Case Summary: An 81-year-old woman with a history of bipolar disorder presented to the emergency department with complaints of fever, chills, nausea, and headache. Two weeks prior to presentation, liver enzymes were normal. Lamotrigine 50 mg/day and sustained-release bupropion 200 mg/day were started after discontinuation of citalopram. The patient had previous exposure to bupropion and documented rash with exposure to penicillin and sulfa. On admission, laboratory tests revealed slightly elevated liver enzymes and slightly low serum albumin. All medications were continued. On hospital day 3, a diffuse maculopapular rash developed on the patient's chest, abdomen, neck, and upper extremities, which was pruritic and warm to the touch. Both lamotrigine and bupropion were discontinued. Liver enzymes increased to more than 3 times the upper limit of normal, and serum albumin decreased. Liver function tests improved on day 6, and the rash resolved. Discussion: Predictive risk factors associated with lamotrigine-induced rash and liver dysfunction include rapid dose titration, previously reported rash with other medications, age, and concurrent interacting medications. More serious adverse effects, such as Stevens–Johnson syndrome and fulminant hepatic failure, have also been associated with lamotrigine treatment. If rash appears at any time during treatment, lamotrigine must be discontinued. According to the Naranjo probability scale, an association between lamotrigine and rash and liver dysfunction could be considered probable in this case. Conclusions: A faster than recommended dose titration may lead to lamotrigine-induced adverse effects such as rash and liver dysfunction in patients with risk factors.

Estudio retrospectivo de la efectividad de la lamotrigina en monoterapia para el tratamiento de crisis epilépticas. Estudio ERELMO

The efficacy and tolerability of lamotrigine (LTG) in monotherapy and in combination therapy have been demonstrated in clinical trials. The aim of the ERELMO study was to retrospectively evaluate the effectiveness and safety of LTG, as monotherapy in the control of epileptic seizures in routine clinical practice in Spain. 446 clinical records were selected of patients with LTG treatment in the twelve months previously to the beginning of the study. The main endpoints retrospectively analyzed were effectiveness (percentage of patients with 50% or greater reduction in seizure frequency, improvement in seizure control, percentage of patients remaining-seizure free at 2, 6 and 12 months of LTG monotherapy), and safety (adverse event profile reported and treatment withdrawal). The mean age was 41 years old, 57.8% were women. LTG monotherapy treatment (mean maintenance dose was 217.2 mg/day) reduced mean seizure frequency as compared with the basal condition at different study time points (2, 6, 12 months; p < 0.0001). At the end of the study 77% of the patients were seizure free. Loss of treatment effectiveness was shown in 8.5% of patients. Adverse reactions were reported by 15% of patients, the most frequent being insomnia, somnolence, headache and rash. At the end of the study, 88.8% patients were still receiving LTG monotherapy. The present study supports the use of LTG monotherapy due to its effectiveness and good tolerability to promote treatment compliance in usual clinical conditions in patients with epilepsy.

Lamotrigine Treatment of Pathologic Skin Picking

Although pathologic skin picking is a relatively common behavior, treatment data are limited. We hypothesized that lamotrigine would reduce the symptoms of pathologic skin picking. 24 subjects (19 women [79.2%]; mean +/-SD age = 34.1 +/- 12.2 years) with pathologic skin picking (based on DSM-IV criteria for other impulse control disorders) were treated in a 12-week open-label trial of lamotrigine as mono-therapy. Lamotrigine dosing ranged from 25 mg every other day to 300 mg/day. The primary outcome measure was time per day spent picking. Subjects were also assessed with measures examining the symptoms of pathologic skin picking and psychosocial functioning. Data were collected from January 15, 2006, to September 18, 2006. Mean (SD) time per day spent picking decreased from 118.1 (130.0) to 59.9 (115.2) minutes (p < .001). Sixteen subjects (66.7%) were considered either "very much improved" or "much improved" in terms of skin picking symptoms. Seven subjects (29.2%) reported no picking at study endpoint. Significant improvement was seen on scales assessing the symptoms of pathologic skin picking (p = .001) and social functioning (p = .002). Mean time to response (i.e., when the subject was much or very much improved) was 8 weeks, which corresponded to a lamotrigine dose of 200 mg/day. Lamotrigine was associated with improvements in two thirds of subjects with pathologic skin picking. Placebo-controlled, double-blind studies are needed to evaluate further the safety, tolerability, and efficacy of lamotrigine in the treatment of this problematic behavior. ClinicalTrials.gov identifier NCT00269594 (http://www.clinicaltrials.gov).

Monotherapy of Lamotrigine Versus Carbamazepine in Patients With Poststroke Seizure

The incidence of seizures is known to be high in the elderly. The most common cause of an unprovoked seizure in the elderly population is stroke. These patients require effective and well-tolerated antiepileptic treatment because they frequently experience other medical conditions and use other medications that can interact with the antiepileptic treatment. The aim of the study was to analyze the tolerability and efficacy of lamotrigine (LTG) versus sustained-release carbamazepine (CBZ) treatment in newly diagnosed symptomatic poststroke seizure. Sixty-four patients with a first post episode of seizures were randomized in a 1:1 ratio to either LTG or CBZ treatment and were followed up prospectively for up to 12 months for efficacy and tolerability of the drugs. More patients in the LTG group were seizure-free (72%) versus those in the CBZ group (44%; P = 0.06), but the numbers did not reach statistical significance because of a relative small number of study patients. The number of patients who withdraw from the study because of adverse events was statistically significantly less in the LTG group (3%) compared with the CBZ group (31%; P = 0.02). The LTG treatment in poststroke seizures versus CBZ treatment is a relatively better-tolerated drug and can be acceptable as initial treatment in this specific group of patients.

Sodium valproate versus lamotrigine: A randomised comparison of efficacy, tolerability and effects on circulating androgenic hormones in newly diagnosed epilepsy

We have performed a randomised, prospective study to compare the efficacy and tolerability of sodium valproate (VPA) and lamotrigine (LTG) monotherapy, and their effects on circulating androgenic hormones, in newly diagnosed epilepsy. A total of 225 patients (116 male; median age 35 years, range 13-80 years) were followed-up at 6-weekly intervals until they reached an end-point (12 months' seizure freedom; withdrawal due to intolerable side-effects; lack of efficacy despite adequate dosing). Twelve month seizure-free rates were identical (47%) in the VPA (n=111) and LTG (n=114) treatment arms. More patients taking VPA withdrew from the study due to adverse events (26 VPA versus 15 LTG; p=0.046). Eight patients, all taking VPA, dropped out during the first 6 months due to weight gain. There were no changes in mean serum concentrations of testosterone, sex-hormone binding globulin and androstenedione or in the free androgen index after 6 or 12 months' treatment with either drug in 112 patients who fulfilled the criteria for hormone analysis. No difference in efficacy was found between VPA and LTG in our patients with newly diagnosed epilepsy. LTG appeared to be better tolerated. Neither drug appeared to alter the circulating levels of androgenic hormones.

Development of psychosis in patients with epilepsy treated with lamotrigine: Report of six cases and review of the literature

Lamotrigine (LTG) is a generally well-tolerated antiepileptic drug (AED) with broad-spectrum efficacy in several forms of partial and generalized epilepsy and is also licensed for use in bipolar disorder in several countries. We describe six patients who developed a psychotic disorder—in most, but not all, cases schizophrenia-like in character—under treatment with LTG, within a group of about 1400 patients treated with this drug in our center. This indicates that psychosis is a rare adverse event under LTG treatment. On the background of available drug serum levels, we suggest, in particular, an intrinsic or toxic psychotogenic effect of LTG. Possible risk factors seem to be psychiatric comorbidity and temporal lobe pathology. The described phenomenon is discussed within the context of possible psychotogenic effects of other AEDs.

Possible New Causes For False-Positive Diagnosis of Pheochromocytoma

Sir: Pheochromocytomas are rare neuroendocrine tumors diagnosed by elevated plasma and/or urine catecholamines or their metabolites.1,2 Medications reported to cause false-positive serum or urine studies include acetaminophen, phenoxybenzamine, amitriptyline, labetolol, haloperidol, levodopa, tamsulosin, venlafaxine, hydrochlorothiazide, and buspirone.2,3 We report a case in which lamotrigine, aripiprazole, or both caused symptoms and biochemical evidence suggesting pheochromo-cytoma that resolved when the drugs were discontinued. There are no previous reports of lamotrigine or aripiprazole associated with false-positive biochemical testing for pheochromocytoma. Case report. Mr. A, a 60-year-old white man, presented in May 2005 with anxiety, palpitations, and panic attacks starting 3 months prior to evaluation, immediately after he underwent cardiac bypass surgery. He had no medical complications peri-operatively and initially attributed his symptoms to the stress of surgery. He was seen by Psychiatry and diagnosed with depression, attention-deficit/hyperactivity disorder, and bipolar disorder and placed on treatment with aripiprazole, lamotrigine, and venlafaxine. Mr. A's attacks became more frequent, and he felt incapacitated. On examination, he appeared anxious. His blood pressure was 141/96 mm Hg, and his pulse was 97 bpm. The remainder of his examination was unremarkable. Additional medical history of the patient included hypothyroidism, hypertension, and obstructive sleep apnea. At initial presentation to the Division of Diabetes, Endocrinology and Metabolism, 3 months after his first evaluation by Psychiatry, his medications were lamotrigine, venlafaxine, and aripiprazole in addition to tamsulosin, aspirin, levothyroxine, amlodipine, benazepril, and rosuvastatin. He was taken off tamsulosin and venlafaxine to undergo biochemical testing for pheochromocytoma. Laboratory tests showed elevated urine and plasma normetanephrines (Table 1). Abdominal computed tomography scan and metaiodobenzyl-guanidine (MIBG) scan findings were normal. Table 1. Biochemical Workup for Pheochromocytoma We discontinued lamotrigine and aripiprazole treatment and repeated plasma and urine studies 3 weeks later, at which time results of Mr. A's plasma and urine studies had normalized, and his symptoms had resolved (Table 1). Lamotrigine is an antiseizure medication, and aripiprazole is a new atypical antipsychotic; both are used in the treatment of bipolar disorder. Lamotrigine prolongs the refractory phase of voltage-gated sodium channels.4 Aripiprazole is a partial D2 agonist and acts differently from the existing atypical antipsy-chotics.5 Neither drug has an obvious mechanism for raising catecholamines or its metabolites. Given the severity of our patient's symptoms, both drugs were stopped simultaneously. His laboratory values returned to normal, and his symptoms resolved completely. He is unwilling to reintroduce each medication separately to determine if the effect observed was an individual drug effect or a synergistic occurrence. Additional reports are needed to evaluate this further. Given this case, we recommend considering lamotrigine and aripiprazole as 2 additional medications that could cause a false-positive biochemical result when evaluating for pheochromocytoma. Dr. Goldner has received honoraria from Abbott and Takeda and has been a member of the speakers/advisory board for Takeda.

Lamotrigine therapy in elderly patients with epilepsy, bipolar disorder or dementia

In spite of circumstances that precipitate high use of anticonvulsants in geriatric populations, there is a paucity of data on the use of antiepileptic drugs in elderly patients with psychiatric and neurological disorders. Reports of lamotrigine therapy in elderly patients with epilepsy, bipolar disorder (BD), or dementia were identified by conducting an electronic search of major publication databases. Abstracts and presentations from professional meetings were searched as were the bibliographies of relevant articles. Fourteen reports were identified, and included well-controlled prospective trials, retrospective analyses, and case reports of lamotrigine treatment. Controlled trials in elderly patients with epilepsy demonstrate efficacy and tolerability comparable to gabapentin. Improvement in bipolar depressive symptoms, improvement in core manic symptoms, and delay in mood relapse was reported in geriatric patients with BD. Preliminary case studies in patients with dementia note improvement in cognition and symptoms of agitation and depression. Review of the available literature suggests lamotrigine is effective and well tolerated in elderly patients with epilepsy and relatively well-tolerated and may be effective in delaying mood relapse, particularly in the depressive pole, in patients with BD. While very limited literature suggests that lamotrigine may be effective and relatively well-tolerated in patients with dementia, further studies are needed.

An Association of Intrusive, Repetitive Phrases with Lamotrigine Treatment in Bipolar II Disorder

Bipolar disorder is frequently associated with obsessional symptoms. However, no reports have identified a pattern of obsessionality that is associated with a specific mood stabilizer treatment. A chart review was conducted on five patients with bipolar II disorder who spontaneously reported a form of obsessionality characterized by intrusive, recurrent phrases after taking lamotrigine. Development of the phrases occurred from 7-42 years after mood disorder onset and occurred only after initiation of lamotrigine treatment. The phrases improved with lamotrigine discontinuation or dose reduction and recurred with lamotrigine re-challenge or upon dose escalation. A possible mechanism for the development of the intrusive phrases involves the influence of lamotrigine on glutamatergic regulation in a bipolar II disorder population vulnerable to the expression of obsessionality. Limitations of this report include its observational nature, small number of cases reported, and confound of concomitant medication use.

Improvement in quality of life after initiation of lamotrigine therapy in patients with epilepsy in a naturalistic treatment setting

Quality of life is impaired in patients with epilepsy and can be improved by effective therapy. Randomised clinical trials have shown that lamotrigine treatment is associated with improved quality of life. However, little information is available on quality of life or treatment effects in patients with epilepsy in the general population. The objective of this study was to estimate the impact of lamotrigine on quality of life in a naturalistic treatment setting. The study included adult patients with epilepsy in whom lamotrigine therapy was initiated. Each subject completed the Quality of Life in Epilepsy Inventory (QOLIE)-31 quality of life questionnaire at inclusion and at a follow-up visit in the next 4 months. Demographic information and medical history were provided by the investigator. These were evaluated as potential determinants of change in quality of life using logistic regression. Three hundred and forty-one patients were evaluated, 192 starting lamotrigine in combination with another drug, 90 as a first-line monotherapy, 45 as a switch from another drug and 14 as a reduction to monotherapy from a previous combination. Baseline scores on the QOLIE-31 ranged from 53.8 in the combination group to 69.5 in the first-line group. 34.6% of patients were considered to be responders, with no significant differences between treatment regimen. Most improvement was seen for the energy-fatigue and medication effects subscales and, for the first-line group, seizure worry. Seizure type was the only determinant of improvement of quality of life identified. In conclusion, lamotrigine treatment is associated with improved quality of life, regardless of treatment regimen.

Lamotrigine in patients with epilepsy and comorbid depressive symptoms

Purpose This open-label study evaluated the antidepressant qualities of lamotrigine (LTG) in people with epilepsy. Methods Eligible patients exhibited low to moderate depressive symptoms and required a change in antiepileptic drug (AED) therapy, but were excluded if they had a major depressive disorder (MDD). Lamotrigine was added onto a stable AED regimen, and self-report instruments were administered to evaluate changes in mood states. Evaluations were conducted at baseline, at the end of 19 weeks of adjunctive treatment, and 36 weeks following conversion to monotherapy. Results One hundred and fifty-eight patients with epilepsy participated; 96 patients completed adjunctive treatment, and 66 patients completed monotherapy. Intent-to-treat analyses for all instruments showed improvement in depression scores after adjunctive LTG treatment. Improvement was maintained for those converted to monotherapy. Conclusions These data suggest that LTG may have antidepressant activity for patients with epilepsy and comorbid low to moderate depressive symptoms, and warrant a randomized controlled trial for validation.

Axonal protection achieved in a model of multiple sclerosis using lamotrigine

Axonal degeneration is a major cause of permanent disability in multiple sclerosis (MS). Recent observations from our and other laboratories suggest that sodium accumulation within compromised axons is a key, early step in the degenerative process, and hence that limiting axonal sodium influx may represent a mechanism for axonal protection in MS. Here we assess whether lamotrigine, a sodium channel-blocking agent, is effective in preventing axonal degeneration in an animal model of MS, namely chronic-relapsing experimental autoimmune encephalomyelitis (CR-EAE). When administered from 7 days post-inoculation, lamotrigine provided a small but significant reduction in the neurological deficit present at the termination of the experiments (averaged over three independent experiments; vehicle: 3.5+/-2.7; lamotrigine: 2.6+/-2.0, P<0.05) and preserved more functional axons in the spinal cord (measured as mean compound action potential area; vehicle: 31.7 microV.ms+/-23.0; lamotrigine: 42.9+/-27.4, P<0.05). Histological examination of the thoracic spinal cord (n=71) revealed that lamotrigine treatment also provided significant protection against axonal degeneration (percentage degeneration in dorsal column; vehicle: 33.5 %+/-38.5; lamotrigine: 10.4 %+/-12.5, P<0.01). The findings suggest that lamotrigine may provide a novel avenue for axonal protection in MS.

Incidence and Time Course of Subsyndromal Symptoms in Patients With Bipolar I Disorder

Subsyndromal symptoms in bipolar disorder can cause significant functional impairment and are associated with relapse. In this post hoc analysis from 2 randomized, double-blind, 18-month, placebo-controlled maintenance trials for bipolar I disorder (both trials were conducted between August 1997 and August 2001 and used DSM-IV criteria), the incidence, time course, and impact of pharmacotherapy on subsyndromal symptoms were examined. Subsyndromal symptoms occurred in approximately 25% of all visits. Compared with placebo (54.8%), a significantly higher mean percentage of visits in remission were observed with lamotrigine treatment (63.0%, p = .020) but not with lithium treatment (60.0%, p = .165). The median time to onset of subsyndromal symptoms for lamotrigine (N = 223), lithium (N = 164), and placebo (N = 188) was 15, 15, and 9 days, respectively. Compared with placebo, both lamotrigine and lithium significantly delayed the time from randomization to onset of subsyndromal symptoms (p = .046, lamotrigine vs. placebo; p = .033, lithium vs. placebo; p = .763, lamotrigine vs. lithium) and the time from onset of subsyndromal symptoms to subsequent mood episode (p = .037, lamotrigine vs. placebo; p = .023, lithium vs. placebo; p = .845, lamotrigine vs. lithium). Agreement between the polarities of the first-observed subsyndromal symptom and subsequent intervention for mood episode was statistically significant (p < .001). Subsyndromal symptoms are common during maintenance treatment and appear to be associated with relapse into an episode of the same polarity. Both lithium and lamotrigine delayed the onset of subsyndromal symptoms and the time from onset of subsyndromal symptoms to subsequent relapse. Further study to assess whether treatment intervention can minimize subsyndromal symptoms or prevent relapse is encouraged.

Effect of Adjunctive Lamotrigine Treatment on the Plasma Concentrations of Clozapine, Risperidone and Olanzapine in Patients With Schizophrenia or Bipolar Disorder

The effect of lamotrigine on the steady-state plasma concentrations of the atypical antipsychotics clozapine, olanzapine, and risperidone was investigated in patients with schizophrenia or bipolar disorder stabilized on chronic treatment with clozapine (200-500 mg/day; n = 11), risperidone (3-6 mg/day; n = 10) or olanzapine (10-20 mg/day; n = 14)). Lamotrigine was titrated up to a final dosage of 200 mg/day over 8 weeks, and pharmacokinetic assessments were made at baseline and during treatment weeks 6 and 10, at lamotrigine dosages of 100 and 200 mg/day respectively. The plasma concentrations of clozapine, norclozapine, risperidone, and 9-hydroxy-risperidone did not change significantly during treatment with lamotrigine. The mean plasma concentrations of olanzapine were 31 +/- 7 ng/mL at baseline, 32 +/- 7 ng/mL at week 6, and 36 +/- 9 ng/mL at week 10, the difference between week 10 and baseline being statistically significant (P < 0.05). Adjunctive lamotrigine therapy was well tolerated in all groups. These findings indicate that lamotrigine, at the dosages recommended for use as a mood stabilizer, does not affect the plasma levels of clozapine, risperidone, and their active metabolites. The modest elevation in plasma olanzapine concentration, possibly due to inhibition of UGT1A4-mediated olanzapine glucuronidation, is unlikely to be of clinical significance.

Variation in Lamotrigine Plasma Concentrations with Hormonal Contraceptive Monthly Cycles in Patients with Epilepsy

This is the first report comparing intrasubject lamotrigine (LTG) plasma concentrations between hormonal contraceptive (HC) intake and week-off phases in epilepsy patients receiving combined LTG and HC treatment. We describe the variation in LTG plasma concentrations with hormonal contraceptive (HC) monthly intake cycles in a series of eight patients with epilepsy. Venous blood samples were prospectively drawn from patients before their first morning dose of LTG, once between days 18 and 21 of HC intake and once between days 5 and 7 of the HC-free week. Median LTG plasma concentrations were significantly higher during the HC washout week than during the phase of HC intake (p = 0.02). The median value of intrasubject percentage increase was 27%, with a wide interpatient variability. These findings are in line with a preliminary report on healthy volunteers. Standardization of blood sampling in relation to HC intake cycles is advisable when planning LTG therapeutic monitoring in patients receiving HC.

Regional Effects of Lamotrigine on Cerebral Glucose Metabolism in Idiopathic Generalized Epilepsy

Antiepileptic drugs have been reported to affect cerebral metabolism. We performed (18)F-fluorodeoxyglucose positron emission tomography (PET) before and after lamotrigine administration to investigate its effects on cerebral glucose metabolism in patients with drug-naïve idiopathic generalized epilepsy. We included patients who were newly diagnosed as having idiopathic generalized epilepsy or who had not taken an antiepileptic drug after the diagnosis was made. Antiepileptic drug (18)F-fluorodeoxyglucose PETs were obtained before and after lamotrigine administration in 21 subjects (male-female ratio, 10:11; mean +/- SD age, 24.3 +/- 2.8 years). The mean lamotrigine dosage was 211.9 mg/d (range, 175.0-275.0 mg/d). For statistical parametric mapping analysis, all PET images were spatially normalized to the standard PET template and then smoothed using a 14-mm full width at half-maximum gaussian kernel. The paired t test was used to compare premedication and postmedication (18)F-fluorodeoxyglucoae PET images. After lamotrigine administration, cerebral metabolism was decreased in bilateral thalami, bilateral caudate nuclei, the left side of the putamen, the left entorhinal area, bilateral parahippocampal gyri, the right inferior temporal gyrus, the left rectosubcallosal gyrus, bilateral superior frontal gyri, the left middle frontal gyrus, the right precentral gyrus, left pericentral gyri, the right superior parietal lobule, and bilateral substantia nigra at P<.05 corrected for multiple comparisons using the false discovery rate approach. No brain region showed increased metabolism after lamotrigine administration. This study revealed that lamotrigine treatment reduces glucose metabolism in the thalamus, basal ganglia, and multiple regions of the cerebral cortex in drug-naïve patients with idiopathic generalized epilepsy.

Localized Purpura Associated With Lamotrigine

Antiepileptic drug hypersensitivity syndrome consists of fever, rash, and internal organ involvement and usually occurs within the first 2 months of initiation of therapy. This report describes a 13-year-old female with a right frontal high-grade glioma and complex partial seizures who developed localized purpura after 23 months of lamotrigine monotherapy. This case study is the second report of localized purpura after prolonged lamotrigine treatment suggesting this may be an atypical lamotrigine-induced drug reaction.

Hair Loss as a Side Effect of Lamotrigine Treatment

Hair Loss as a Side Effect of Lamotrigine Treatment

Hair Loss as a Side Effect of Lamotrigine Treatment

Hair Loss as a Side Effect of Lamotrigine Treatment

True Epilepsy Unmasked in a Case of Apparent Conversion Disorder

Sir: The prevalence of psychogenic nonepileptic seizures is estimated to be between 2 and 33 per 100,000 persons.1 We describe a patient in whom a difficult case of apparent conversion but true epilepsy was unmasked by video-electroencephalogram (video-EEG) monitoring. Case report. Ms. A, a 40-year-old white woman, presented to the neurology clinic with a 2-year history of intermittent spells of disorientation and memory loss. She described these spells as a wavelike sensation starting in her stomach and rising up into her chest, after which she would “blank out” for about a minute or so and then for the next 15 to 20 minutes would ask questions like “Where am I?” “What day is it?” “Am I married?” and “Do I have children?” During these periods, she gradually became more responsive and eventually would become increasingly responsive until the disorientation abated completely. Most of these episodes would occur in her house in the presence of her husband and occasionally in front of her children. She would have no recollection of the event. At no point during these episodes would she lose consciousness or have fecal or urinary incontinence or tongue biting. She denied seeing an aura or any knowledge of exacerbating or relieving factors. These spells could occur as frequently as 10 times in a month, but sometimes a couple of weeks would pass without any episode. Since her first spell 2 years before the admission described in the current report, she had been seen by her primary care physician, neurologist, psychiatrist, and psychologist several times. Occasional complete neurologic examinations revealed no focal findings. Results of a computed tomography scan and magnetic resonance imaging of the head as well as an EEG showed no evidence of intracranial pathology or any epileptogenic activity. EEG testing was repeated several times over the 2-year period and revealed no seizure activity. Her general blood chemistry findings and thyroid profile had also been within normal limits. There was no history of head trauma, febrile seizures, meningitis, or encephalitis and no family history of seizures. Substance use history was nonsignificant. Her medical history was significant for hypertension, which was under good control with amlodipine, 5 mg once daily. She had also been diagnosed with depression for the same period of time and had undergone a trial of venlafaxine, which produced minimal benefits. At the present admission, the depression was under fair control with paroxetine, 60 mg daily. On presentation to our clinic, Ms. A was admitted for video-EEG monitoring, which recorded 1 of her spells. When correlated with the EEG findings, the video-EEG findings revealed left hemispheric slowing with an epileptiform discharge that gradually spread to the bilateral hemispheres. She was then started on lamotrigine treatment for seizure prevention, which led to significant improvement within a few weeks. Around 10% to 20% of patients are found to have both epilepsy and psychogenic nonepileptic seizures.2 Although video-EEG is not widely accepted by psychiatrists, it is considered to be a standard of care for making a diagnosis of psychogenic nonepileptic seizures.2 Obtaining a definite diagnosis and separating seizure disorder from psychiatric disorder is critical, as the treatment for each is different and an early intervention for seizure disorder is essential.3 Failure to treat a true seizure disorder can lead to devastating physical and psychological complications.