Seizures Of Frontal Lobe Origin Research Articles

Semiology of hyperkinetic seizures of frontal versus temporal lobe origin.

Hyperkinetic seizures are usually associated with frontal lobe epilepsy. However, some patients have hyperkinetic seizures of temporal lobe origin. The semiological differences in hyperkinetic seizures between frontal and temporal lobe epilepsy have not been well studied. Here, we retrospectively assessed ictal semiology in order to distinguish between hyperkinetic seizures of frontal lobe origin and those of temporal lobe origin. We retrospectively reviewed data on patients who had undergone surgery for hyperkinetic seizures of temporal or frontal lobe origin and achieved favourable seizure outcomes (Engel Class I) with a minimum postoperative follow-up of 24 months. We reviewed seizure histories, imaging reports, video-EEG monitoring data, operative records, and pathological findings. We analysed and compared the hyperkinetic semiology of video-recorded seizures of temporal lobe origin and those of frontal lobe origin. Forty hyperkinetic seizures in eight patients (seven adult patients and one 12-year-old patient) with temporal lobe epilepsy and 45 hyperkinetic seizures in nine patients (eight adult patients and one 16-year-old patient) with frontal lobe epilepsy were analysed. Emotional facial expressions (such as fear, laughing, or anger), bilateral forceful elbow flexion, bilateral forceful grasping, facial flushing, and bilateral facial contraction were observed significantly more frequently in seizures of frontal lobe origin. Oroalimentary automatisms, seizures during wakefulness, salivation, and bilateral drop of the corners of the mouth were observed significantly more frequently in seizures of temporal lobe origin. Observation of a number of signs during hyperkinetic manifestations may help to predict whether a seizure originates from the frontal lobe or the temporal lobe.

History of frontal lobe seizures

Any historical review of seizures originating in the frontal lobes (FLS) is faced with several difficulties: the huge diversity of ictal manifestations, from the most simple myoclonic event originating in the elementary precentral motor cortex, to very bizarre and misleading phenomena, involving associative cortices and widely distributed networks, that were not rarely misinterpreted as psychogenic attacks (Tharp [1] ); the often unclear relationship between semiologic patterns and sublobar localization in spite of many attempts to characterize typical anatomical-clinical-electrical patterns that would be typical of a given sub region, like the orbito-frontal or medial frontal lobe areas [2] , [3] ; the different terminologies employed to characterize FLS, reflected in the evolving classifications of the International League Against Epilepsy (ILAE) between 1981 and 2017. FLS are often brief, sometimes a few seconds, due to the rapid propagation pathways which are offered inside and outside the frontal lobe to the epileptic discharge , making the observation and the analysis difficult, although seizures in a given patient with frontal lobe epilepsy are generally stereotyped, with a stable and reproducible electro-clinical pattern. And last but not least, FLS are often nocturnal, without obvious electroencephalographic (EEG) correlations, and have been often in the past misdiagnosed as parasomnia . The manifestations include: paroxysmal arousals, characterized by brief and sudden recurrent motor paroxysmal behavior; nocturnal paroxysmal dystonia, motor attacks with complex dystonic–dyskinetic features; and episodic nocturnal wanderings, stereotyped, agitated somnambulism. The recognition of their epileptic nature led to the terminology of Nocturnal Frontal Lobe Epilepsy, and a familial clustering permitted the discovery of several pathogenic gene variants [4] , [5] . In spite of this complexity, the study of frontal lobe seizures has largely contributed to our understanding of the pathophysiology of epileptic discharges: the first description of focal clonic seizures by J.F. Bravais in 1827, then Hughlings Jackson in 1867, who related clonic seizures to electric discharges in the contralateral precentral region and described a “march”, this stepwise invasion of neighboring areas of the motor cortex by the ictal discharge, with progressive somatotopic engagement of limb musculature. Other frontal lobe seizure types , however, showed that this march phenomenon cannot be considered as a universal model of emergence and spreading of the discharge. Supplementary motor area seizures producing speech arrest (a negative phenomenon), unilateral arm posturing, and head or eye deviation, later referred to as “fencing posture” by Penfield [6] , illustrate rapid modalities of subcortical propagation. Using stereoencephalography , Bancaud and Talairach [2] defined frontal lobe automatisms , and detailed descriptions of complex partial seizures of frontal lobe origin followed with P. Williamson et al. [7] . The term “hypermotor seizure” was also proposed. In the revised ILAE classification, FLS are classified as “focal seizures” with further descriptors such as “either aware or with impaired awareness”, or “with or without observable motor components” [8] . Frontal lobe seizures with secondary generalization are now described as focal evolving to bilateral tonic-clonic seizures .

Familial partial epilepsy with variable foci: A new family with suggestion of linkage to chromosome 22q12

Familial partial epilepsy with variable foci (FPEVF) is an autosomal dominant form of partial epilepsy characterized by the presence of epileptic seizures originating from different cerebral lobes in different members of the same family. Linkage to chromosomes 22q12 and 2q36 has been reported, although only six families have been published. We studied a new FPEVF family including nine affected individuals. The phenotype in this family was similar to that previously described and consisted of nocturnal and daytime seizures with semiology suggesting a frontal lobe origin. A video-EEG (electroencephalography) recording of the proband's seizures is presented and revealed hyperkinetic seizures of frontal lobe origin preceded by left frontal spikes. We excluded linkage to chromosome 2q36 and found a suggestion of linkage to chromosome 22q12 with a lod score of 2.64 (h = 0) for marker D22S689.

Gelastic seizures: A case of lateral frontal lobe epilepsy and review of the literature

We describe a 40-year-old patient with gelastic seizures triggered by hand movement. Despite nonlesional magnetic resonance imaging (MRI), electroencephalography (EEG), functional magnetic resonance imaging (fMRI), and diffusion tensor imaging (DTI) are concordant with seizure onset in the right frontocentral area. Seizure semiology and EEG recordings imply involvement of mesial frontal structures remote from seizure initiation site. We reviewed all published cases on gelastic seizures of frontal lobe origin to find characteristic features. For further investigation of the phenomenon of movement-induced seizures, fMRI was performed using a finger tapping paradigm. Interictal fMRI revealed widespread activation of right motor cortex during finger tapping on either side outreaching the anatomical representation of the left finger. In line with this finding DTI revealed fiber track impairment in the right frontocentral region, supporting the hypothesis of a focal derangement. This case highlights the importance of complementary functional investigations in MRI-negative epilepsies.

To Sleep, Perchance to Seize: Surgery Ameliorates Nocturnal Frontal Lobe Seizures

Surgical Treatment of Drug-resistant Nocturnal Frontal Lobe Epilepsy. Nobili L, Francione S, Mai R, Cardinale F, Castana L, Tassi L, Sartori I, Didato G, Citterio A, Colombo N, Galli C, Lo Russo G, Cossu M. Brain 2007;130 (Pt 2):561–573. Of the cases with nocturnal frontal lobe epilepsy (NFLE) 30% are refractory to antiepileptic medication, with several patients suffering from the effects of both ongoing seizures and disrupted sleep. From a consecutive series of 522 patients operated on for drug-resistant focal epilepsy, 21 cases (4%), whose frontal lobe seizures occurred almost exclusively (>90%) during sleep, were selected. All patients underwent a comprehensive pre-surgical evaluation, which included history, interictal EEG, scalp video-EEG monitoring, high-resolution MRI and, when indicated, invasive recording by stereo-EEG (SEEG). There were 11 males and 10 females, whose mean age at seizure onset was 6.2 years, mean age at surgery was 24.7 years and seizure frequency ranged from <20/month to >300/month. Nine patients reported excessive daytime sleepiness (EDS). Prevalent ictal clinical signs were represented by asymmetric posturing (6 cases), hyperkinetic automatisms (10 cases), combined tonic posturing and hyperkinetic automatisms (4 cases) and mimetic automatisms (1 case). All patients reported some kind of subjective manifestations. Interictal and ictal EEG provided lateralizing or localizing information in most patients. MRI was unrevealing in 10 cases and it showed a focal anatomical abnormality in one frontal lobe in 11 cases. Eighteen patients underwent a SEEG evaluation to better define the epileptogenic zone (EZ). All patients received a microsurgical resection in one frontal lobe, tailored according to pre-surgical evaluations. Two patients were operated on twice owing to poor results after the first resection. Histology demonstrated a Taylor-type focal cortical dysplasia (FCD) in 16 patients and an architectural FCD in 4. In one case no histological change was found. After a post-operative follow-up of at least 12 months (mean 42.5 months) all the 16 patients with a Taylor's FCD were in Engel's Class Ia and the other 5 patients were in Engel's Classes II or III. After 6 months post-surgery EDS had disappeared in the 9 patients who presented this complaint pre-operatively. It is concluded that patients with drug-resistant, disabling sleep-related seizures of frontal lobe origin should be considered for resective surgery, which may provide excellent results both on seizures and on epilepsy-related sleep disturbances. An accurate pre-surgical evaluation, which often requires invasive EEG recording, is mandatory to define the EZ. Further investigation is needed to explain the possible causal relationships between FCD, particularly Taylor-type, and sleep-related seizures, as observed in this cohort of NFLE patients.

Nocturnal Frontal Lobe Epilepsy: There is Bad, Good, and Very Good News!

Surgical Treatment of Drug-Resistant Nocturnal Frontal Lobe Epilepsy. Nobili L, Francione S, Mai R, Cardinale F, Castana L, Tassi L, Sartori I, Didato G, Citterio A, Colombo N, Galli C, Lo Russo G, Cossu M. Brain 2007;130(Pt 2):561–573. Of the cases with nocturnal frontal lobe epilepsy (NFLE) 30% are refractory to antiepileptic medication, with several patients suffering from the effects of both ongoing seizures and disrupted sleep. From a consecutive series of 522 patients operated on for drug-resistant focal epilepsy, 21 cases (4%), whose frontal lobe seizures occurred almost exclusively (>90%) during sleep, were selected. All patients underwent a comprehensive pre-surgical evaluation, which included history, interictal EEG, scalp video-EEG monitoring, high-resolution MRI and, when indicated, invasive recording by stereo-EEG (SEEG). There were 11 males and 10 females, whose mean age at seizure onset was 6.2 years, mean age at surgery was 24.7 years and seizure frequency ranged from <20/month to >300/month. Nine patients reported excessive daytime sleepiness (EDS). Prevalent ictal clinical signs were represented by asymmetric posturing (6 cases), hyperkinetic automatisms (10 cases), combined tonic posturing and hyperkinetic automatisms (4 cases) and mimetic automatisms (1 case). All patients reported some kind of subjective manifestations. Interictal and ictal EEG provided lateralizing or localizing information in most patients. MRI was unrevealing in 10 cases and it showed a focal anatomical abnormality in one frontal lobe in 11 cases. Eighteen patients underwent a SEEG evaluation to better define the epileptogenic zone (EZ). All patients received a microsurgical resection in one frontal lobe, tailored according to pre-surgical evaluations. Two patients were operated on twice owing to poor results after the first resection. Histology demonstrated a Taylor-type focal cortical dysplasia (FCD) in 16 patients and an architectural FCD in 4. In one case no histological change was found. After a post-operative follow-up of at least 12 months (mean 42.5 months) all the 16 patients with a Taylor's FCD were in Engel's Class Ia and the other 5 patients were in Engel's Classes II or III. After 6 months post-surgery EDS had disappeared in the 9 patients who presented this complaint pre-operatively. It is concluded that patients with drug-resistant, disabling sleep-related seizures of frontal lobe origin should be considered for resective surgery, which may provide excellent results both on seizures and on epilepsy-related sleep disturbances. An accurate pre-surgical evaluation, which often requires invasive EEG recording, is mandatory to define the EZ. Further investigation is needed to explain the possible causal relationships between FCD, particularly Taylor-type, and sleep-related seizures, as observed in this cohort of NFLE patients.

Further evidence of genetic heterogeneity in families with autosomal dominant nocturnal frontal lobe epilepsy

Purpose Mutations in the genes encoding the alfa 2, alfa 4 and beta 2 subunits of the neuronal nicotinic acetylcholine receptor (nAChR) play a causative role in autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE). Moreover, variations in the promoter of the corticotropic-releasing hormone gene ( CRH) were also associated with ADNFLE. Here, we investigated whether nine brain-expressed genes ( CHRNA2, CHRNA3, CHRNA4, CHRNA5, CHRNA6, CHRNA7, CHRNB2, CHRNB3, CHRNB4), encoding distinct nAChR subunits, and CRH are associated with the disease in three distinct ADNFLE families from Southern Italy. Methods There were 14 living affected individuals (9 women), ranging in age from 14 to 57 years, pertaining to three unrelated families. Age at onset of seizures clustered around 9 years of age (range from 7 and 16 years, mean: 9.1 years ± 3.8). All affected individuals manifested nocturnal partial seizures of frontal lobe origin, which were well controlled by medications. Exon 5 of CHRNA4 and CHRNB2 genes, harboring all the known mutations, was sequenced in the probands. Then, we performed a linkage study on 13 affected and 26 non-affected individuals belonging to the three families with microsatellite markers and an intragenic polymorphisms encompassing the chromosome localization of the nAChR subunit genes and of the CRH gene. Results Mutational and linkage analyses allowed us to exclude the involvement of all known nAChR subunit genes and of the CRH gene in ADNFLE in our families. Conclusion Our results further illustrate the considerable genetic heterogeneity for such a syndrome, despite the quite homogeneous clinical picture. It is therefore reasonable to hypothesize that at least another gene not belonging to the nAChR gene family, in addition to CRH, is involved in the pathogenesis of ADNFLE.

Surgical treatment of drug-resistant nocturnal frontal lobe epilepsy

Of the cases with nocturnal frontal lobe epilepsy (NFLE) approximately 30% are refractory to antiepileptic medication, with several patients suffering from the effects of both ongoing seizures and disrupted sleep. From a consecutive series of 522 patients operated on for drug-resistant focal epilepsy, 21 cases (4%), whose frontal lobe seizures occurred almost exclusively (>90%) during sleep, were selected. All patients underwent a comprehensive pre-surgical evaluation, which included history, interictal EEG, scalp video-EEG monitoring, high-resolution MRI and, when indicated, invasive recording by stereo-EEG (SEEG). There were 11 males and 10 females, whose mean age at seizure onset was 6.2 years, mean age at surgery was 24.7 years and seizure frequency ranged from <20/month to >300/month. Nine patients reported excessive daytime sleepiness (EDS). Prevalent ictal clinical signs were represented by asymmetric posturing (6 cases), hyperkinetic automatisms (10 cases), combined tonic posturing and hyperkinetic automatisms (4 cases) and mimetic automatisms (1 case). All patients reported some kind of subjective manifestations. Interictal and ictal EEG provided lateralizing or localizing information in most patients. MRI was unrevealing in 10 cases and it showed a focal anatomical abnormality in one frontal lobe in 11 cases. Eighteen patients underwent a SEEG evaluation to better define the epileptogenic zone (EZ). All patients received a microsurgical resection in one frontal lobe, tailored according to pre-surgical evaluations. Two patients were operated on twice owing to poor results after the first resection. Histology demonstrated a Taylor-type focal cortical dysplasia (FCD) in 16 patients and an architectural FCD in 4. In one case no histological change was found. After a post-operative follow-up of at least 12 months (mean 42.5 months) all the 16 patients with a Taylor's FCD were in Engel's Class Ia and the other 5 patients were in Engel's Classes II or III. After 6 months post-surgery EDS had disappeared in the 9 patients who presented this complaint pre-operatively. It is concluded that patients with drug-resistant, disabling sleep-related seizures of frontal lobe origin should be considered for resective surgery, which may provide excellent results both on seizures and on epilepsy-related sleep disturbances. An accurate pre-surgical evaluation, which often requires invasive EEG recording, is mandatory to define the EZ. Further investigation is needed to explain the possible causal relationships between FCD, particularly Taylor-type, and sleep-related seizures, as observed in this cohort of NFLE patients.

Cardiac asystole during right frontal lobe seizures: a case report

The association between partial seizures and cardiac asystole has rarely been reported in the literature. This potentially life-threatening symptom has been observed principally in left-sided epilepsies, in particular during seizures originating in temporal lobe. We describe a case with ictal bradycardia followed by cardiac asystole during right frontal lobe seizures. Video-EEG monitoring recorded two partial seizures with electro-clinical findings suggestive of a right frontal lobe origin, associated with ictal bradycardia followed by prolonged asystole. The brain MRI showed a lesion located in the cingulate gyrus of the right frontal lobe. The patient required a subsequent placement of a pacemaker. In conclusion, cardiac asystole may be a potentially life-threatening symptom during seizures of frontal lobe origin. The right fronto-mesial structures may play a role in autonomic regulation of cardiovascular responses.

Etiology, diagnosis, and treatment of nonepileptic seizures.

Psychogenic nonepileptic seizures (NES) can be classified into five categories. This review focuses on NES associated with emotional conflict, by far the most common and important group. Etiology is speculative, but the background histories of these patients are often similar. The presence of a trauma history, depression, post-traumatic stress symptoms, and the use of dissociation plus cognitive dysfunction possibly point to an organic etiology. The presentation of NES in children and adults is discussed, along with the differential diagnosis. The diagnostic differential is lengthy, with epileptic seizures of frontal lobe origin presenting a unique challenge. Diagnostic procedures are reviewed with an emphasis on the utility of hypnosis with seizure induction. Presenting the diagnosis to the patient, the role of the neurologist, and the role of the mental health consultant are reviewed. Issues in the doctor-patient relationship are also addressed, as well as the overall prognosis.

Frontal Localization of Absence Seizures Demonstrated by Ictal Positron Emission Tomography

Generalized absence seizures are rarely reported to originate from one frontal lobe. We report an 8-year-old girl with atypical absence seizures demonstrated to be of right frontal origin by ictal positron emission tomography (PET). She had a congenital left hemiparesis and intractable seizures since age 3, and was referred for epilepsy surgery. During electroencephalography-video monitoring numerous episodes of atypical absence seizures were recorded in association with generalized 3- to 3.3-Hz spike-and-wave discharges by EEG. PET was performed with simultaneous EEG recording. Six typical seizures occurred during the fluorodeoxyglucose (FDG) uptake period. The PET scan demonstrated marked increased FDG uptake in right frontal region. Partial seizures of frontal lobe origin can manifest themselves as atypical absence seizures, with generalization based on secondary bilateral synchrony. In patients with frequent seizures the frontal seizure origin may be demonstrated noninvasively with functional imaging using PET or single-photon emission computed tomography.

A new locus for autosomal dominant nocturnal frontal lobe epilepsy maps to chromosome 1.

Autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is caused by mutations in the alpha4 subunit of the neuronal nicotinic acetylcholine receptor (CHRNA4) gene, mapping on chromosome 20q13.2. A second ADNFLE locus was mapped on chromosome 15q24. To report a new third ADNFLE locus on chromosome 1 in a large Italian family. The authors performed a clinical and genetic study in a large, three-generation ADNFLE family from southern Italy, including eight affected individuals and three obligate carriers. The age at onset of seizures was around 9 years of age and all affected individuals manifested nocturnal partial seizures of frontal lobe origin. Interictal awake and sleep EEG recordings showed no definite epileptiform abnormalities in most patients. Ictal video-EEG showed that the attacks were partial seizures with a frontal lobe semiology. Intellectual and neurologic examinations, and brain CT or MRI results were always normal. Carbamazepine was effective in all treated patients. Exclusion mapping of the known loci linked to ADNFLE-ENFL1, and ENFL2, on chromosomes 20q13.2 and 15q24-was performed on the pedigree before starting the genome-wide linkage analysis. The whole genome scan mapping allowed the identification of a new ADNFLE locus spanning the pericentromeric region of chromosome 1. The authors provided evidence for a third locus associated to autosomal dominant nocturnal frontal lobe epilepsy on chromosome 1. Among the known genes mapping within this critical region, the ss2 subunit of the nicotinic receptor (CHRNB2) represents the most obvious candidate.

Intractable seizures of frontal lobe origin: clinical characteristics, localizing signs, and results of surgery.

We analyzed the clinical characteristics of seizures of frontal lobe (FL) origin with particular emphasis on establishing different categories and determining if these categories had any localizing or lateralizing value. In addition, results of surgery are reported. Seizure characteristics were established by historical review and electroencephalographic/videotape analysis of 449 seizures in 26 adult patients with refractory seizures of FL origin. No outstanding risk factor was identified for seizures of FL origin. Seizures were frequent (7.1 per week), brief (mean duration, 48.3 seconds), and had a nocturnal preponderance in 58% of the patients. Status epilepticus was reported in 54%, and generalized convulsions as a prominent seizure type were reported in 26% of patients. The most common reported aura was a nonspecific sensation, often localized to the head (35%). Early forced head and eye deviation was not a consistent lateralizing sign, whereas late head and eye deviation always occurred contralateral to the site of seizure origin. Early asymmetric tonic posturing occurred consistently contralateral to the side of seizure origin. Clinical seizure patterns did not consistently localize to specific regions of the frontal lobe, although there were some noticeable trends: focal clonic seizures were associated with seizure origin in the frontal convexity; tonic seizures were most often associated with origin in the supplementary motor area but also occurred with origin in other parts of the frontal lobe; seizures resembling typical temporal lobe seizures with oroalimentary automatisms were observed with seizure origin in the orbitofrontal region; and seizures with hyperactive, frenetic automatisms were not associated with any specific region within the frontal lobes. Eighty percent of patients had favorable seizure outcome after surgery (class I/II). Although certain clinical features are characteristic for seizures of frontal lobe origin and some have lateralizing value, they do not localize to specific areas within the FL. After careful presurgical evaluation, both lesional and nonlesional patients benefit from epilepsy surgery.

A unique effect of clonazepam on frontal lobe seizure control

In a 16-year-old female, clonazepam (CZP) changed randomly occurring intractable tonic seizures of frontal lobe origin to a few sleep seizures when used as an adjunctive therapy. The significance of this change in the seizure pattern is discussed with an explanation of possible pathophysiologic mechanism.

Neuropsychological Differences in Epileptic Patients With Seizures of Frontal and Temporal Lobe Origin

This investigation studied the neuropsychological di8erences in nonsurgical cryptogenic epileptic patients with seizures of frontal and temporal lobe origin, which were classified according to clinical criteria. Fifty-one patients with partial seizures of frontal (n = 15) or temporal (n = 36) lobe origin and 2 matched control groups were administered a battery of neuropsychological tests assessing intelligence, memory, perceptual, and frontal functions. Patients with seizures of temporal lobe onset performed worse than patients with seizures of frontal lobe origin, even in frontal functions. The findings of this study corroborate the low specificity of tasks regarded as frontal lobe tests and the difficulty in detecting frontal lobe neuropsychological focalities.

Frontal lobe epilepsy: Clinical syndromes and presurgical evaluation

Our understanding of the anatomy and function of the brain's frontal lobe has increased steadily. In the last 8 years, two major meetings, one in 1987 and the other in 1993, have been devoted to this subject alone (1,2). However, despite intense clinical and basic science research, much is still unknown concerning the functional anatomy of the frontal lobe. There are significant implications for the epileptologist to understand the different clinical manifestations and to localize seizures of frontal lobe origin. Factors that limit the study of the frontal lobe include its anatomic size, its extensive networking with other parts of the brain, as well as its limited access to scalp EEG recording. Recent advances in technology are improving the methods available to study the frontal lobe. These new technologies include expanded EEG channels, including supraorbital and nasoethmoidal electrodes, computerized EEG analysis, and intracranial intraoperative and chronic recording, single photon emission computed tomography (SPECT), positron emission tomography (PET), magnetic resonance imaging (MRI), and neuropsychological testing. A consensus remains to be established among different epilepsy centers regarding the use of a systematic approach in evaluation of patients

Electrophysiology of bimanual-bipedal automatisms.

To determine the localizing value and electrophysiology of bimanual-bipedal automatisms (BBAs), we studied these behaviors in 54 seizures of 8 patients with temporal or frontal lobe seizure onset. BBAs occurred with a frequency of 27% in frontal lobe epilepsy (FLE) and of 7% in temporal lobe epilepsy (TLE). The distribution of electrode sites showing ictal activity during these automatisms was significantly different in the two patient groups (0.0001 Chi-square). Mesio- and/or laterotemporal plus orbital frontal areas were involved areas when the behaviors appeared in patients with TLE; dorsolateral and mesiofrontal regions were the most commonly involved when the behaviors occurred during the course of frontal lobe seizures. We concluded that BBAs represent activation of frontal lobe circuitry but are not unique to seizures of frontal lobe origin. Eyelid flutter and repetitive body movements in either the axial or sagittal plane were significantly associated with the frontal lobe group whereas oral-alimentary automatisms were associated with the temporal lobe group. Thus, these associated behaviors may help indicate whether a frontal or temporal lobe seizure onset has occurred when BBAs are observed. A new concept of ictal expression is proposed to conform with the results as well as with other apparently disparate ictal behaviors that may have localizing value.

Rotatory seizures of frontal lobe origin

We report a patient with true rotatory seizures. The CT scan showed a right frontal calcified lesion and the EEG showed focal epileptiform discharges over the right frontal region. The seizures responded well to phenytoin therapy.

FRONTAL LOBE COMPLEX PARTIAL SEIZURES IN CHILDREN: A FORM OF EPILEPSY AT PARTICULAR RISK OF MISDIAGNOSIS

The clinical and EEG findings are described of six children considered to have complex partial seizures of frontal lobe origin. The findings correspond generally with those reported for adult patients. Video-recordings of attacks in some cases and ictal cassette EEG recordings provided important diagnostic information. A definite frontal abnormality on neuro-imaging was seen in only one case. The seizures were closely associated with sleep, and anti-epileptic drug treatment was usually of limited value. The considerable diagnostic confusion surrounding seizures of this type, including their misdiagnosis as pseudoseizures or primary sleep disorder, is partly the result of the clinical peculiarities of this type of seizure, but also of clinicians' limited awareness of the condition.

Behavioral Complications of Frontal Lobe Seizures

A 13-yr-old girl with marked behavioral and selective cognitive deficits associated with partial complex seizures of frontal lobe origin is reported from the Depts of Neurology, Psychiatry and Pediatrics, Harbor-UCLA Medical Center, 1000 W Carson St, Torrance, CA.