Seizure-free Period Research Articles

The demographic, clinical and forensic profile of offenders diagnosed with epilepsy referred to the Free State Psychiatric Complex Observation Unit in terms of section 77 and/or 78 of the Criminal Procedure Act 51 of 1977

<p><strong>Introduction.</strong> Limited information regarding the relation between psychopathology associated with epilepsy, crime and the legal aspects thereof is available in South Africa.</p><p><strong>Objectives:</strong> The demographic, clinical and forensic profile of alleged offenders diagnosed with epilepsy and referred to the Free State Psychiatric Complex (FSPC) Observation Unit from 2001 to 2006, was investigated. Design A retrospective cross-sectional study was conducted.</p><p><strong> Results:</strong> Of the 69 alleged offenders, aged 17–79 years (median 30 years), 94.2% were male, 81.2% Black, 72.5% single, and 69.9% unemployed. The median qualification was grade six. Offences were violent in nature and committed against a person in 75% of cases. A direct link between epilepsy and the alleged offences occurred in 7% of cases. Generalised epilepsy (34.8%) and interictal psychosis (20.3%) were the most commonly diagnosed conditions. Twenty-nine (42%) alleged offenders lacked criminal responsibility and were not fit to stand trial. Most observati (79.2%) diagnosed with generalised epilepsy were criminally liable and fit to stand trial. The highest rate of criminal incapacity was found among observati with interictal psychoses (85.7%) and comorbid mental retardation (90%). Almost 60% of referred cases were declared as state patients by the court.</p><p><strong>Conclusion:</strong> In only 16% of cases, observati were found unaccountable because of epilepsy (automatisms) or postictal confusional states. Our findings confirmed an increased prevalence of violent behaviour during seizure-free periods. This contributes to evidence that factors associated with epilepsy, rather than the epilepsy itself, play an important role in the possible increased risk of violent behaviour in people with epilepsy.</p>

Epileptic nystagmus: Description of a pediatric case with EEG correlation and SPECT findings

Epileptic nystagmus (EN) describes repetitive eye movements that result from seizure activity. We describe a patient with EN and vertigo first noted at the age of 4 yr and 10 mo. Brain MRI did not show anomalies. Ictal EEG recordings revealed epileptic activity during three episodes of horizontal, left-beating nystagmus not crossing the midline. Ictal 99mTc-ECD SPECT demonstrated the presence of active foci in multiple cerebral regions including bilateral prefrontal, bilateral parieto-temporo-occipital and the left parieto-insular-vestibular areas. A wide area of hypoperfusion was also evident in the right hemisphere, prevailing in the parieto-occipital regions and the medial prefrontal gyrus. Topiramate was started at a dose of 2 mg/kg/d with complete seizure control after 14 d. EEG and SPECT were repeated after a seizure-free period of 1 mo; disappearance of epileptic activity and modification of cerebral perfusion were evident. This case reaffirms the cortical origin and involvement of temporo-occipital and frontal cortex in the genesis of saccadic epileptic nystagmus. Rapid complete control of clinical events coincided with the normalization of EEG and improvement of the SPECT pattern.

The burden experienced by family caregivers of patients with epilepsy attending the government psychiatric hospital, Kaduna, Nigeria

Caring for patients with chronic medical and psychiatric disorders is associated with significant burden. However little is known about the burden experience by caregivers of patients with epilepsy in Nigeria. The objective of this study, therefore, was to assess the level and correlates of burden among caregivers of patients with epilepsy. It was a cross-sectional study carried out among 231 eligible caregivers of patients with epilepsy attending the psychiatric clinic of government psychiatric hospital in Kaduna, Northern Nigeria. Sociodemographic/clinical characteristics of patients and socio-demographic characteristics of caregivers were recorded, and the Zarit Burden Interview administered to caregivers to assess their experience of burden. The mean age of the caregivers was 43.6 ± 9.5 years, 52.4% lived outside Kaduna and the mean seizure-free period for the patients was 26.4 ± 36.5 weeks. One hundred and twenty (51.9%) caregivers had high burden. High burden was significantly associated with patients aged less than 20 years, patient's unemployment, long duration of epilepsy, short seizure-free period, family history of epilepsy and living outside Kaduna (p value<0.05). Caregivers of patients with epilepsy experience significant burden while caring for their relatives and this is mainly associated with patient's factors and location of residence. Therefore efforts should be made control seizure and make health care available and affordable to all citizens irrespective of where they live.

Gastaut type-idiopathic childhood occipital epilepsy and childhood absence epilepsy: A clinically significant association?

We report an unusual association between idiopathic occipital epilepsy and childhood absence epilepsy in 2 pediatric patients. At first clinical and electroencephalographic evaluation, the patients presented the peculiar signs of idiopathic occipital epilepsy Gastaut type: focal sensory visual seizures, migraine-like symptoms (only in one patient) and unilateral spike–wave discharges over occipital regions. Both children were treated with valproic acid and their seizures were rapidly controlled. After a seizure-free period, the patients presented typical absence with ictal electroencephalographies showing 3 cycles/s generalized and symmetrical spike–wave complexes. We discuss the possible association between these two epileptic syndromes and its common pathophysiological mechanisms.

90. Three-year follow-up of patients with epilepsy after thediscontinuation of antiepileptic drugs

Objective: The purpose of this study was to examine the rate of relapse of epileptic seizures in patients with epilepsy, in whom antiepileptic drugs (AEDs) were discontinued after a seizure free period of 3 years.

Determination of risk factors associated with seizure relapse after antiepileptic drug withdrawal

Abstract There is no consensus regarding the time of antiepileptic drug withdrawal and the relevant risk factors for seizure relapse. In this study, we aimed to determine the seizure relapse rates and the associated risk factors for seizure relapse in childhood epilepsy. Two-hundred sixty-six epileptic patients who discontinued the antiepileptic drug therapy after a seizure-free period of at least two years, were enrolled into the study. The data of the patients regarding sex, febrile convulsion history, family history, age at onset, type of epilepsy, total number of seizures and antiepileptic drugs, seizures during treatment, mental status, first and last electroencephalography, brain imaging findings, etiological factors and seizure relapse in the first two years after antiepileptic drug withdrawal were obtained from the patients’ files. Univariate logistic regression analysis was performed for each variable. The variables which were found to be statistically significant in univariate analysis, were included in multivariate logistic regression analysis. The overall seizure relapse rate after antiepileptic drug withdrawal was 19.2%. There were no significant differences for seizure relapse rate after antiepileptic drug withdrawal between patient groups with respect to sex, family history, type of epilepsy, febrile convulsion history, seizures before treatment, first electroencephalography findings, brain imaging findings and etiology. However, there were statistically significant differences for seizure relapse rate among patient groups concerning age at onset of epilepsy, new seizure during treatment, the total number of antiepileptic drugs, mental status, and last electroencephalography findings. We imply that the clinical status of the patients should be considered before the cessation of drug therapy rather than the etiological factors or laboratory findings.

EPILEPSY IN CHILDREN WITH INFANTILE THIAMINE DEFICIENCY

Objective: To report the follow-up findings of 7 children with severe epilepsy as a result of thiamine deficiency in infancy caused by a defective soy-based formula. Methods: The medical records of 7 children aged 5-6 years with thiamine deficiency in infancy who developed epilepsy were reviewed and their clinical data, EEG tracings, and neuroimaging results were recorded. The clinical course and present outcome of these children, now 5 years after exposure to thiamine deficiency, are described. Results: All infants displayed seizures upon presentation, either tonic, myoclonic, or focal. Six infants had an EEG recording at this stage and all showed slow background. Five of them had no epileptic activity and only 1 displayed focal activity. Following a seizure-free period of 1-9 months, the seizures recurred, and all 7 children displayed either myoclonic or complex partial seizures. Multifocal or generalized spike wave complexes were recorded on the EEGs of all 7 patients, and the tracings of 3 children evolved into hypsarrhythmia. The seizures were refractory to most antiepileptic drugs, and 4 children remain with uncontrolled seizures. All children have mental retardation and motor disabilities as well as symptoms of brainstem dysfunction. Conclusions: Our findings indicate that severe infantile thiamine deficiency may result in epilepsy.

Risk of recurrence after a first seizure and implications for driving: further analysis of the Multicentre study of early Epilepsy and Single Seizures

Objective To determine for how long after a first unprovoked seizure a driver must be seizure-free before the risk of recurrence in the next 12 months falls below 20%, enabling...

Social consequences of epilepsy: A study of 231 Nigerian patients

Epilepsy is the commonest neurological disorder and majority of the sufferers are found in the developing countries. It is associated with psychological and social problems. The aim of this study was to determine the social difficulties experienced by epileptic patients and the factors that are associated with these difficulties. Two hundred and thirty-one consecutive epileptic patients who were of age 10 years and above, and who had no co-morbid major psychiatric disorder, seen over a 6-month period at the outpatient clinic of Federal Neuro-psychiatric Hospital, Kaduna, were interviewed. We used an instrument designed for the purpose of this study, which focused on people's attitudes to epilepsy, relationship/marital, employment and academic problems. The mean age of the subjects was 28 +/- 13.2 years; 59.3% were males; 44.6% said people make negative remarks about their illness; 14.1% have been denied leadership role; 36.4% were irregular at work; 37.3% performed poorly at work; 22.5% have had their marriage proposals rejected; 19.5% have been abandoned by spouse. At least 39.4% had poor academic performance while 19.5% were withdrawn from school because of epilepsy. Short seizure-free period, long duration of seizure disorder and family history of epilepsy were significantly associated with social problems. Social difficulties are common among epileptics. Effort should be made to educate the society about epilepsy, and physicians treating patients with epilepsy should aim at achieving a good seizure control.

Natural history of solitary cerebral cysticercosis cases after albendazole therapy: a longitudinal follow-up study from India

To find out natural course of solitary cerebral cysticercosis (SCC) cases after treating them with 2 weeks albendazole therapy. All patients with SCC were treated with 2 weeks of albendazole therapy with follow-up radiological scan at 6 months and 2 years. The evolution of lesion was noted as complete resolution, calcification or persistent active. Antiepileptic drugs (AED) prophylaxis was given for 1 year in patients with complete resolution and for 2 years in calcified lesion, respectively. AED was continued in persistent lesion group till it became calcified or resoluted completely. One-year follow-up was done in all after stopping AED. Among 345 cases, 226 (65.5%) had complete resolution with very low seizure relapse rate with 1 year of seizure free period on AED treatment. On the contrary, 105 (30.5%) had calcified lesion with high seizure relapse rate after stopping AED treatment with 2 years of seizure free period. Fourteen patients (4%) could not stop their antiepileptic medication at all because of active lesion. Two-third of patients with SCC have favorable outcome with complete resolution and needs short-term AED prophylaxis and the rest one-third requires long AED treatment to prevent seizures.

Hemiconvulsion–hemiplegia syndrome in a patient with severe myoclonic epilepsy in infancy

We report a 2-year-old girl who had repeated febrile or afebrile seizures since infancy. Prolonged left/right hemiconvulsions and myoclonus of the eyelids/extremities with generalization to tonic-clonic seizures, were refractory to antiepileptic agents. At age 1 year and 4 months, she contracted rotavirus infection, and developed status epilepticus with persistent right hemiclonic seizures. Left unilateral brain edema with subsequent emergence of cortical laminar necrosis and white matter lesions, and progressive atrophy of the left cerebral hemisphere were noted during this period. She showed residual right hemiparesis and mild intellectual disability, and had generalized/eyelid myoclonia and hot water epilepsy after a 5-month seizure-free period. Analysis for SCN1A, the gene encoding the neuronal voltage-gated Na+ channel alpha1 subunit revealed a nonsense mutation, R1892X. These indicate the potential risk in patients with severe myoclonic epilepsy in infancy (SMEI) to develop hemiconvulsion-hemiplegia (HH) syndrome. SCN1A mutations may need to be further explored in patients with HH syndrome without features of SMEI.

An infantile‐onset, severe, yet sporadic seizure pattern is common in Sturge‐Weber syndrome

The young age of onset and frequently intractable nature of seizures associated with Sturge-Weber syndrome (SWS) have been well-reported in large studies. However, many clinicians also anecdotally describe prolonged but sporadic seizure clusters. Over a 5-year period, 77 children and adults with SWS and at least one reported seizure were referred to and evaluated at the Hunter Nelson Sturge-Weber Center at the Kennedy Krieger Institute. The median age of seizure onset was 6 months with 43 (56%) presenting <1 year of age. Age at seizure onset < or = 6 months was associated with increased hemiparesis, but not seizures. A characteristic pattern of clustering, intense seizures followed by prolonged seizure-free periods was reported in 30 (39%), but was not associated with worse prognosis. This seizure pattern appears to be common with SWS and leads to difficult treatment decisions, especially in regard to the timing of potential surgical resection.

Epilepsy in children with infantile thiamine deficiency

To report the follow-up findings of 7 children with severe epilepsy as a result of thiamine deficiency in infancy caused by a defective soy-based formula. The medical records of 7 children aged 5-6 years with thiamine deficiency in infancy who developed epilepsy were reviewed and their clinical data, EEG tracings, and neuroimaging results were recorded. The clinical course and present outcome of these children, now 5 years after exposure to thiamine deficiency, are described. All infants displayed seizures upon presentation, either tonic, myoclonic, or focal. Six infants had an EEG recording at this stage and all showed slow background. Five of them had no epileptic activity and only 1 displayed focal activity. Following a seizure-free period of 1-9 months, the seizures recurred, and all 7 children displayed either myoclonic or complex partial seizures. Multifocal or generalized spike wave complexes were recorded on the EEGs of all 7 patients, and the tracings of 3 children evolved into hypsarrhythmia. The seizures were refractory to most antiepileptic drugs, and 4 children remain with uncontrolled seizures. All children have mental retardation and motor disabilities as well as symptoms of brainstem dysfunction. Our findings indicate that severe infantile thiamine deficiency may result in epilepsy.

Pathological alterations in GABAergic interneurons and reduced tonic inhibition in the basolateral amygdala during epileptogenesis

An acute brain insult such as traumatic head/brain injury, stroke, or an episode of status epilepticus can trigger epileptogenesis, which, after a latent, seizure-free period, leads to epilepsy. The discovery of effective pharmacological interventions that can prevent the development of epilepsy requires knowledge of the alterations that occur during epileptogenesis in brain regions that play a central role in the induction and expression of epilepsy. In the present study, we investigated pathological alterations in GABAergic interneurons in the rat basolateral amygdala (BLA), and the functional impact of these alterations on inhibitory synaptic transmission, on days 7 to 10 after status epilepticus induced by kainic acid. Using design-based stereology combined with glutamic acid decarboxylase (GAD) 67 immunohistochemistry, we found a more extensive loss of GABAergic interneurons compared to the loss of principal cells. Fluoro-Jade C staining showed that neuronal degeneration was still ongoing. These alterations were accompanied by an increase in the levels of GAD and the α1 subunit of the GABAA receptor, and a reduction in the GluK1 (previously known as GluR5) subunit, as determined by Western blots. Whole-cell recordings from BLA pyramidal neurons showed a significant reduction in the frequency and amplitude of action potential–dependent spontaneous inhibitory postsynaptic currents (IPSCs), a reduced frequency but not amplitude of miniature IPSCs, and impairment in the modulation of IPSCs via GluK1-containing kainate receptors (GluK1Rs). Thus, in the BLA, GABAergic interneurons are more vulnerable to seizure-induced damage than principal cells. Surviving interneurons increase their expression of GAD and the α1 GABAA receptor subunit, but this does not compensate for the interneuronal loss; the result is a dramatic reduction of tonic inhibition in the BLA circuitry. As activation of GluK1Rs by ambient levels of glutamate facilitates GABA release, the reduced level and function of these receptors may contribute to the reduction of tonic inhibitory activity. These alterations at a relatively early stage of epileptogenesis may facilitate the progress towards the development of epilepsy.

Partial Seizures With Secondary Generalization While on Treatment With Clozapine and Sertraline

Sir: Clozapine is known to cause generalized and myoclonic seizures. Here we report a neurologically normal individual who developed partial seizures with secondary generalization while receiving clozapine and sertraline. Case report. Mr. A, a 19-year-old man with paranoid schizophrenia whose psychotic symptoms had remitted with clozapine (300 mg/day), presented in 2007 with severe obsessive impulses to jump from heights. He had unremarkable birth and developmental history and had no past or family history of neurologic illness including epilepsy. He had never used psychoactive substances. His physical examination was normal. He was started on treatment with sertraline 50 mg/day, which was increased to 100 mg/day after 4 days; clozapine was continued at 300 mg/day. A week after the sertraline dose was increased to 100 mg/day, his mother noticed twitching of the angle of his mouth, which deviated toward the left with jerky movements of facial muscles. This was followed, within seconds, by a generalized tonic-clonic seizure lasting for about 2 minutes. He regained consciousness after about 5 minutes. He was treated with intravenous phenytoin and subsequently (the next day) prescribed oral phenytoin (300 mg/day) and quetiapine (200 mg/day); clozapine and sertraline were discontinued. Magnetic resonance imaging (MRI) of the brain revealed no lesion that could explain focal seizures. Electroencephalograms (EEGs) recorded immediately following seizure and after 2 days were normal. He reported that he had involuntary twitching movements of his face toward the left starting on the day after sertraline treatment was begun. These lasted for a few seconds and occurred about 7 to 8 times a day, but he had not reported it until he had a generalized seizure. Partial seizures decreased in frequency and stopped within a week; they did not recur while the patient was on treatment with quetiapine, which was built up to 800 mg/day over 2 weeks, along with phenytoin at 300 mg/day. Phenytoin was tapered and stopped after a 2-month seizure-free period. A diagnosis of seizure induced by combination of clozapine and sertraline was made. This case illustrates that clozapine may cause partial seizures in neurologically normal patients. History, examination, and MRI revealed no neurologic problems. Seizures had not occurred while the patient was taking only 300 mg/day of clozapine but occurred immediately after adding sertraline. Sertraline can increase plasma clozapine level.1,2 Since clozapine's epileptogenic property is dose dependent, this effect could induce seizures. Alternatively, sertraline could have independently put the patient at risk for development of seizures.3 About 10% of patients treated with any dose of clozapine develop seizures.4 However, partial seizures due to atypical antipsychotics either have been associated with brain lesions5–7 or have not been investigated for an association with such lesions.7 We investigated our patient for possible focal lesions but could find none. Hypotheses that attempt to explain the epileptogenic properties of clozapine mainly apply to the generalized seizures.7 One theory posits that clozapine increases rapid eye movement (REM) sleep and that a compensatory non-REM mechanism occurring during the wakeful state causes seizures. Another theory implicates mesolimbic selectivity of clozapine to explain its epileptogenic property.7 Neither theory explains generation of partial seizures. The seizure threshold–lowering property of clozapine could have activated some micro-epileptogenic focus not detected by EEG and MRI in our patient. At this stage, this explanation remains hypothetical. Systematic analysis of EEGs and clinical seizures of clozapine-treated patients that looks specifically for evidence of the focal nature of the seizures may clarify whether clozapine can cause partial seizures in the absence of focal lesions. Our patient did not complain of partial seizures until he developed a generalized seizure. It is possible that, in many patients, such partial seizures caused by clozapine could go unnoticed. It is tempting to hypothesize that partial seizures may be harbingers of generalized seizures in some patients, and if so, clinicians should have a high index of suspicion to look for partial seizures. Further research is needed to investigate this possible connection between partial and generalized seizures. Vivek H. Phutane, M.B.B.S. Channaveerachari Naveen Kumar, M.D., D.P.M. Jagadisha Thirthalli, M.D. Department of Psychiatry Seemendra Kumar Mahato, M.D. Department of Neuro Radiology Sanjib Sinha, M.D., D.M. Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore, India

Early-onset seizure variant of Rett syndrome: Definition of the clinical diagnostic criteria

Background: Rett syndrome is a severe neurodevelopmental disorder affecting almost exclusively females. Among Rett clinical variants, the early-onset seizure variant describes girls with early onset epilepsy and it is caused by mutations in CDKL5. Methods: Four previously reported girls and five new cases with CDKL5 mutation, ranging from 14 months to 13 years, were evaluated by two clinical geneticists, classified using a severity score system based on the evaluation of 22 different clinical signs and compared with 128 classic Rett and 25 Zappella variant MECP2-mutated patients, evaluated by the same clinical geneticists. Clinical features were compared with previously described CDKL5 mutated patients. Both the statistical and the descriptive approach have been used to delineate clinical diagnostic criteria. Results: All girls present epilepsy with onset varying from 10 days to 3 months. Patients may present different type of seizures both at onset and during the whole course of the disease; multiple seizure types may also occur in the same individual. After treatment with antiepileptic drugs patients may experience a short seizure-free period but epilepsy progressively relapses. Typical stereotypic hand movements severely affecting the ability to grasp are present. Psychomotor development is severely impaired. In the majority of cases head circumference is within the normal range both at birth and at the time of clinical examination. Conclusion: For the practical clinical approach we propose to use six necessary and eight supportive diagnostic criteria. Epilepsy with onset between the first week and 5 months of life, hand stereotypies, as well as severe hypotonia, are included among the necessary criteria.

An Acquired Channelopathy Involving Thalamic T-Type Ca2+Channels after Status Epilepticus

Some epilepsies are linked to inherited traits, but many appear to arise through acquired alterations in neuronal excitability. Status epilepticus (SE) is associated with numerous changes that promote spontaneous recurrent seizures (SRS), and studies have suggested that hippocampal T-type Ca(2+) channels underlie increased bursts of activity integral to the generation of these seizures. The thalamus also contributes to epileptogenesis, but no studies have directly assessed channel alterations in the thalamus during SE or subsequent periods of SRS. We therefore investigated longitudinal changes in thalamic T-type channels in a mouse pilocarpine model of epilepsy. T-type channel gene expression was not affected during SE; however Ca(V)3.2 mRNA was significantly upregulated at both 10 d post-SE (seizure-free period) and 31 d post-SE (SRS-period). Overall T-type current density increased during the SRS period, and the steady-state inactivation shifted from a more hyperpolarized membrane potential during the latent stage, to a more depolarized membrane potential during the SRS period. Ca(V)3.2 functional involvement was verified with Ca(V)3.2 inhibitors that reduced the native T-type current in mice 31 d post-SE, but not in controls. Burst discharges of thalamic neurons reflected the changes in whole-cell currents, and we used a computational model to relate changes observed during epileptogenesis to a decreased tendency to burst in the seizure-free period, or an increased tendency to burst during the period of SRS. We conclude that SE produces an acquired channelopathy by inducing long-term alterations in thalamic T-type channels that contribute to characteristic changes in excitability observed during epileptogenesis and SRS.

SECTION A: CHILDRENS' EPILEPSY

Acta Neurologica ScandinavicaVolume 82, Issue s133 p. 9-11 SECTION A: CHILDRENS' EPILEPSY First published: December 1990 https://doi.org/10.1111/j.1600-0404.1990.tb03939.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Abstract Epilepsy and disorders of skin pigmentation Prognosis in Childhood Epilepsy Seizures in childhood: A prospective community based cohort study Epilepsy in mentally retarded children and adults Birthe Pedersen and M. Dam The value of syndrome classification in childhood epilepsy A follow-up study among children with epilepsy:Treatment, seizure free periods, and educational achievements The use of the “monolog spike and wave monitor to manage antiepileptic treatment Pseudoseizures in children Valproate-induced hyperventilation in a child with therapy-resistant epilepsy Epilepsy and overactivity: Classification and man-agement Volume82, Issues133December 1990Pages 9-11 RelatedInformation

Risk of recurrence after drug withdrawal in childhood epilepsy

Objectives After a reasonable seizure-free period, discontinuation of antiepileptic drugs (AED) is usually decided in epileptic patients despite the risk of seizure recurrence. In children, risk of recurrence after discontinuation of AED is generally 20–40%; however, there is still no general agreement on the criteria to predict safe discontinuation. This study was designed to determine the risk of recurrence and related risk factors after drug withdrawal in epileptic children. Methods 200 epileptic patients between 1 month and 15 years of age who were followed at least 1 year after drug withdrawal at a child neurology center between January 1993 and December 2005 formed the study population of this retrospective study. Patients were classified into groups according to defined risk factors for recurrence. Results Of 200 patients (118 boys, 82 girls), overall recurrence rate was 27%. Girls were more likely to have a seizure recurrence than boys, with the difference approaching statistical significance ( p = 0.058). EEG recordings after withdrawal (post-withdrawal EEG) in the follow-up were significantly different in the patients with recurrence with respect to presence of an abnormality ( p = 0.05). In the multivariate Cox regression analysis, female gender and abnormal post-withdrawal EEG were the risk factors influencing seizure recurrence, with female gender identified as the main risk factor. Conclusions Although the decision to discontinue AED treatment necessitates evaluation of each patient individually, our study suggests that female patients and those with abnormal EEG after withdrawal require more cautious follow-up because of the high risk of recurrence.

Anatomo‐electro‐clinical correlations: the Miami Children's Hospital, USA Case Report ‐ Case 04‐2008: MRI‐negative frontal lobe epilepsy with ipsilateral akinesia and reflex activation

The pre-operative assessment and surgical management of children and young adults with MRI-negative, frontal lobe epilepsy is often challenging owing to the semiologic expression being unusual or non-lateralizing. Localization based on functional tests may be non-convergent, further compounding the difficulty of surgical planning. We describe a patient with seizures presenting with early, subjective akinesia of the dominant hand that were at times triggered by repetitive motor tasks. Subdural EEG monitoring revealed seizure-origin in the ipsilateral dorsolateral frontal lobe. After resective surgery the patient has had a seizure free period of 9 months, and is free of deficits. This is the first report of frontal lobe seizure semiology consisting of ipsilateral ictal akinesia.