Periodic Lateralized Epileptiform Discharges Research Articles

Estado de mal epiléptico no convulsivo secundario a hemorragia subaracnoidea como forma de presentación de una angiopatía amiloide cerebral

Cerebral amyloid angiopathy is a frequent cause of haemorrhagic cerebrovascular disease in persons over the age of 65 and, sometimes, the initial symptoms can be epilepsy-like. A 62-year-old female with no relevant past history who was admitted to hospital due to non-convulsive status epilepticus, auditory hallucinations and ideomotor apraxia; an electroencephalogram performed on the patient revealed periodic lateralised epileptiform discharges in the right parietooccipital region. Susceptibility-weighted magnetic resonance imaging showed a sub-acute focal subarachnoid haemorrhage in the right parietotemporal region and cortico-subcortical microbleeding in different stages of the progression of the disease that were compatible with cerebral amyloid angiopathy. A critical simple single-photon emission tomography scan was performed and findings revealed an area of hyperperfusion in the same region. Antiepileptic treatment was established with clinical, neurophysiological and scintigraphic resolution. The article reports a case with non-convulsive status epilepticus as the initial symptom of cerebral amyloid angiopathy. It also highlights the usefulness of sequences of susceptibility-weighted magnetic resonance imaging and the physiopathogenesis of periodic lateralised epileptiform discharges as an element of epileptic activity is discussed.

How useful is EEG and EEG monitoring in the acutely ill and how to interpret it?

How useful is EEG and EEG monitoring in the acutely ill and how to interpret it?

Prognostic Implications of Periodic Epileptiform Discharges

Periodic epileptiform discharges (PEDs) are an abnormal finding on electroencephalograms (EEGs), the significance of which is uncertain. To investigate long-term outcome in patients with PEDs. We retrospectively analyzed the outcomes of patients who had PEDs diagnosed during a 7-year period. We abstracted and tabulated clinical parameters from the time of EEG, imaging findings, EEG measurements, and subsequent clinical outcome from medical records. We used descriptive, inferential, and logistic regression analysis to determine the factors associated with clinical outcomes in patients with PEDs. We divided PEDs into the following subgroups: periodic lateralized epileptiform discharges (PLEDs), generalized PEDs, and bilateral PEDs and analyzed these subgroups individually. University-affiliated teaching hospital. Subjects One hundred sixty-two patients with PEDs. We obtained complete clinical, neuroimaging, neurophysiologic, and long-term outcome data in 118 patients. In the subgroup of patients with PLEDs, absence of seizures at onset (odds ratio, 0.21 per point; 95% confidence interval, 0.04-0.97) and an acute etiology for the PLEDs (odds ratio, 0.14 per point; 95% confidence interval, 0.03-0.72) were associated with death. A nonneoplastic cause for PLEDs was associated with independent functionality (odds ratio, 0.45 per point; 95% confidence interval, 0.3-0.67). In patients with PLEDs, the absence of clinical seizures at the time of detection and presumed acute etiology are associated with death, whereas a nonneoplastic etiology was associated with a good clinical outcome.

Intravenous levetiracetam: a new treatment alternative for refractory status epilepticus

The purpose of this study was to investigate the safety and efficacy of intravenous levetiracetam (LEV-iv) in refractory status epilepticus (SE). A retrospective chart review was performed on patients who...

Periictal diffusion abnormalities of the thalamus in partial status epilepticus

To identify and describe thalamic dysfunction in patients with temporal as well as extratemporal status epilepticus (SE) and to also analyze the specific clinical, radiological, and electroencephalography (EEG) characteristics of patients with acute thalamic involvement. We retrospectively identified patients who presented with clinical and electrographic evidence of partial SE and had thalamic abnormalities on diffusion-weighted imaging (DWI) within 5 days of documentation of lateralized epileptiform discharges (group 1). The spatial and temporal characteristics of the periodic lateralized epileptiform discharges (PLEDs) and the recorded electrographic seizures were analyzed and correlated with magnetic resonance imaging (MRI)-DWI hyperintense lesions. The findings of group 1 patients were compared with those of patients with partial SE without thalamic abnormalities on DWI (group 2). The two groups were similar with regard to clinical presentation and morphology of epileptiform discharges. Group 1 patients had thalamic hyperintense lesions on DWI that appeared in the region of the pulvinar nucleus, ipsilateral to the epileptiform activity. Statistically significant relationship was noted between the presence of thalamic lesions and ipsilateral cortical laminar involvement (p = 0.039) as well as seizure origin in the posterior quadrants (p = 0.038). A trend towards PLEDs originating in the posterior quadrants was also noted (p = 0.077). Thalamic DWI hyperintense lesions may be observed after prolonged partial SE and are likely the result of excessive activity in thalamic nuclei having reciprocal connections with the involved cortex. The thalamus likely participates in the evolution and propagation of partial seizures in SE.

Predictors of a Prolonged Clinical Course in Adult Patients with Herpes Simplex Virus Encephalitis

Herpes simplex virus encephalitis (HSVE) patients occasionally follow a prolonged course despite standard antiviral treatment. The purpose of this study was to analyze clinical variables to identify predictors of a prolonged course. A series of 23 HSVE patients treated with acyclovir (ACV) during the acute stage were selected and divided into 2 groups: the non-prolonged group (n = 15), with improvement within 2 weeks after initial ACV treatment; and the prolonged group (n = 8), without improvement within 2 weeks. Differences in clinical variables, including age, duration from onset to initial ACV treatment, Glasgow coma scale (GCS) score, corticosteroid administration, detection of abnormal lesions on initial cranial computed tomography (CT) and magnetic resonance imaging, detection of periodic lateralized epileptiform discharges on electroencephalogram, and clinical outcome, were compared between the groups. There were significant differences in GCS score, clinical outcome, and detection of lesions on CT between the non-prolonged and prolonged groups [p = 0.021, p = 0.041 (Mann-Whitney's U test), respectively, and p = 0.027 (Fisher's exact test)]. Four of the eight patients with a prolonged course had a poor outcome despite treatment with additional drugs. A lower GCS and a higher rate of lesions on CT were identified as predictors of a prolonged course for HSVE. These predictors are in accordance with the conventional predictors of poor outcome for HSVE. This study suggests that the initial ACV treatment was insufficient for HSVE patients with these predictors at the acute stage. The initial treatment may need to be modified for such patients.

Symptomatic seizures in neurosyphilis: An experience from a University Hospital in south India

Neurosyphilis has protean clinical manifestations, including epilepsy. However, there is paucity of literature providing details regarding seizures. The aim of the study was to analyze the clinical profile and brain imaging features of 30 patients of neurosyphilis, and to evaluate the predictors and the outcome of seizures in this subgroup. Among the 119 patients (M:F:: 84:35) of neurosyphilis, evaluated over 6 years, 30 patients (M:W::23:7, age: 37.5+/-10.1 years, duration of illness: 11.9+/-20.1 months) were reported to have seizures. CSF-VDRL was positive in all. In addition, HIV serology was positive in 2/20. Seizure was the dominant symptom in all and lone manifestation in two patients. None had history of epilepsy. Their seizure profile was: generalized (17), partial (8), and status epilepticus (5). Concomitant manifestations were encephalopathy (7), meningitis (7), dementia (6), behavioral disturbances (4), stroke (2), and optic atrophy (1). CSF study revealed pleocytosis in 24 (34.6+/-51.5/cu mm) and raised protein in 20 (67+/-33.3mg%). CT scan was abnormal in 26 patients and revealed diffuse atrophy in all and focal hypodensities in 5 patients. MRI of brain (6) showed features of ischemia (2), meningeal enhancement (1) and white matter (1) and medial temporal (2) signal changes. Three patients had reversible periodic lateralized epileptiform discharges (PLEDs), without structural lesion. Nineteen patients received penicillin and/or ceftriaxone. At a mean follow up of 6.7+/-9.4 months, 13/17 had variable improvement. Nine patients required polytherapy and seizures remained uncontrolled in five patients. Symptomatic seizures due to neurosyphilis are frequent, may have diverse underlying mechanism(s) and rarely can be the lone manifestation. In view of availability of specific therapy for syphilis, a high index of suspicion is recommended.

Ictal paresis associated to PLEDS in two children: A video-EEG study

Ictal paresis (IP) is a rare negative motor phenomenon presenting challenging differential diagnostic problems with transient ischemic attacks, post-ictal paralysis, migraine and psychogenic paralysis. Video-EEG undoubtedly represents the essential mean for a proper diagnosis. Periodic lateralised epileptiform discharges (PLEDs) are a distinctive EEG pattern, consisting of periodic spike or sharp wave discharges, often associated with seizures. It is under debate if PLEDs should be considered only a peri-ictal or also an ictal EEG pattern. We describe two children with severe focal epilepsies, who presented IP recorded during video-EEG monitoring, associated to PLEDs. Clinical observation along with interictal and ictal scalp-EEG findings, suggested a fronto-temporal seizure onset in the first, and a temporo-insular onset in the second. We confirm that PLEDs may be an ictal pattern associated with negative motor phenomena.

Limbic encephalitis associated with potassium channel antibodies: demonstration of clinical and paraclinical responses to immunotherapy

Materials and methods We describe the case of a 79-year old patient with symptoms of LE who presented with high fever, affective changes in personality, auditory hallucinations, memory loss, irrelevant talking and confusion. The brain MRI at admission showed a left hippocampal T2-weighted lesion with meningeal gadolinium-enhancement and the EEG showed periodic lateralized epileptiform discharges (PLEDS) on the left temporal area. Routine blood tests were normal. CSF examination at admission revealed 50 cells/mm3, predominantly polynuclear (87%) and 0.74 g/l proteins. Polymerase chain reaction for herpes virus 1 to 3, 6 and enterovirus were negative. The patient was treated with acyclovir but three weeks later he developed myoclonia with secondary generalized epileptic seizures. The serum was negative for paraneoplastic antibodies including Hu, Yo, Ri, CV2/CRMP5, Amphiphysin, Ma2/ Ta. Results Despite the anti-epileptic treatment, the patient's symptoms deteriorated. MRI showed new lesions. The EEG showed a new focus of right parietal PLEDS. Serum voltage-gated potassium channel antibodies (VGKC-Ab) were detected at high levels (3.495 pM). Steroids and plasma exchange were initiated with marked and sustained improvement of neuropsychological function. This clinical improvement correlated with both EEG and radiological amelioration.

Sporadic Creutzfeldt–Jakob disease presenting as stroke mimic

A hypertensive 75-year-old woman with hypertrophic cardiomyopathy, hypercholesterolaemia and paroxysmal atrial fibrillation was referred to the author's neurovascular clinic with sudden onset word-finding difficulty and right-sided weakness. Examination confirmed mild right pyramidal drift and expressive dysphasia in an otherwise relatively independent patient. Computed tomography (CT) confirmed a lacunar infarct involving the posterior limb of the internal capsule (Figure 1). Neurorehabilitation afforded initial improvement, but her family reported deterioration in concentration, coordination and continence control with emotional lability over the next 4 weeks, prompting hospital admission. On examination, she was bedbound, with severe expressive dysphasia (abbreviated mental test score 0/10), dysphagia, global weakness, hypertonia, hyperreflexia and bilateral upper limb myoclonus (more on the right hand side). Repeat CT confirmed previous findings. Lumbar puncture was acellular with a protein count of 0.42 g/dl. Sequential electroencephalograms (EEGs) demonstrated bilateral periodic lateralized epileptiform discharges which were abolished by intravenous lorazepam suggesting nonconvulsive status epilepticus. However, deterioration continued despite antiepileptic therapy. Magnetic resonance imaging demonstrated bilateral putamen and caudate nucleus enhancement on T2 FLAIR with left temporal lobe cortical ribboning on diffusion weighted imaging (Figures 2 and 3). A subsequent EEG showed an evolving picture, with bilateral triphasic waves (1Hz) (Figure 4) compatible with a diagnosis of probable sporadic Creutzfeldt–Jakob disease. This was supported with a positive cerebrospinal fluid 14-3-3 protein assay. The patient died 59 days after the initial presentation. No tissue diagnosis was made.

Epilepsia partialis continua in mitochondrial dysfunction: Interesting phenotypic and MRI observations

An 11-year-old girl manifested with photophobia, ptosis, external ophthalmoplegia, hypotonia, weakness of proximal limb muscles, hyporeflexia, and generalized seizures (six months). Her elder sister had had uncontrolled seizures and photophobia and died at seven years of age. In the patient, serum lactate was high (55 mg/dl). Muscle biopsy revealed characteristic ragged red and ragged blue fibers, diagnostic of mitochondrial cytopathy. Sequencing of the complete mitochondrial genome of the DNA obtained from the muscle biopsy of the patient did not show any characteristic mutation. Four months later, the girl was admitted with a one-week history of epilepsia partialis continua (EPC). EEG revealed Periodic Lateralized Epileptiform Discharges (PLEDs), once in 2-4 seconds, over the right temporo-occipital leads. MRI revealed signal change of right motor cortex, which had restricted diffusion. MR spectroscopy (MRS) from this region revealed lactate peak. EPC remained refractory to multiple anti-epileptic drugs, immuno-modulators, coenzyme-Q, and carnitine. This thought provoking report expands the spectrum of mitochondrial cytopathies.

Periodic Lateralized Epileptiform Discharges in La Crosse Encephalitis, a Worrisome Subgroup: Clinical Presentation, Electroencephalogram (EEG) Patterns, and Long-Term Neurologic Outcome

La Crosse virus encephalitis is the most common mosquito-borne virus in children in the United States. La Crosse virus encephalitis has emerged as a significant health concern due to its potential for acute morbidity, including seizures, alterations in mental status, and, in rare cases, death, as well as the potential for chronic morbidity, including, epilepsy and cognitive and behavioral disorders. The aim of this study is to provide a clinical description of the largest series of children reported with periodic lateralizing epileptiform discharges (PLEDS) associated with La Cross virus encephalitis with reference to their clinical course, seizure type, electroencephalogram (EEG) patterns, and 2- and 10-year long-term neurologic outcome. In addition, to evaluate whether this subset of children may indeed have more severe disease than children with La Crosse virus encephalitis without PLEDS, comparisons are made between the 2 groups on specific variables. All patients presented with fever and disorientation; 6 of the 9 (66%) presented with seizures. PLEDS localized to the temporal lobe in 7 patients (77%). The children with PLEDS had longer intensive care unit stays (6.5 +/- 2.4 vs 3.2 +/- 1.9; P < .0001), a higher rate of intubation (88% vs 20%; P < .001), and a higher rate of cerebral herniation (1%; P < .05) than children with La Crosse virus encephalitis without PLEDS. Follow-up data on the subset with PLEDS also suggest a relatively high rate of epilepsy and behavioral difficulties with hyperactivity symptoms, memory deficits, and school difficulties. The implications for recognition, management, and follow-up of this worrisome subset of patients with La Crosse virus encephalitis are discussed.

Assessment of hairline EEG as a screening tool for nonconvulsive status epilepticus: Response to Bubrick et al.

To the Editors: We thank Dr. Bubrick and her colleagues for interest in our paper. In their letter to Epilepsia (Bubrick et al., 2007), they raise some interesting points for discussion. Overall, they disagree with our conclusions because they feel the sensitivity and specificity for detection of nonconvulsive status epilepticus (NCSE) with a hairline electroencephalogram (EEG) is adequate, and that waiting to obtain a standard EEG will needlessly delay treatment decisions. Moreover, they routinely use this practice and have found it useful (Milligan & Bromfield, 2005). Since the impetus for our study was the delay in obtaining urgent and emergent EEG, we agree that a more rapid assessment would be preferable. Bubrick et al. suggest that the sensitivity and specificity of hairline EEG is adequate for this purpose. In our study, the sensitivity for detecting electrographic seizures was 72% and for periodic lateralized epileptiform discharges (PLED) was only 54% (Kolls & Husain, 2007). Certainly the detection of PLED is very important, since in certain situations it may represent an ictal or interictal pattern. Additionally, a review of the misinterpretations reveals that 33 seizure and 42 PLED patterns were misinterpreted as diffuse slowing (see Figs 3 and 4 in Kolls & Husain, 2007). Moreover, seven patterns with diffuse slowing were misinterpreted as seizures, PLED, or generalized periodic epileptiform discharges (GPED). These are significant errors that may gravely impact patient care. It should also be noted that samples in our study were interpreted by experience neurophysiologists; interpretation by neurology residents resulted in even lower sensitivities and specificities (unpublished data). Consequently, we maintain that a hairline EEG is inadequate for diagnosing NCSE. Bubrick et al. note that patterns of NCSE were not studied. The patterns that were selected, such as electrographic seizures, PLED, and GPED, were not random, and are very likely to be present in patients in NCSE. Identification of these patterns would warrant an emergent EEG and possibly treatment of NCSE. Knowledge of the clinical situation, while always helpful, would be only of marginal additional utility. Bubrick et al. also noted that they have taught the hairline EEG technique to their residents and have found it useful (Milligan & Bromfield, 2005). Unfortunately, the reference cited to support this claim of usefulness includes a single patient who was found to be in NCSE with a hairline EEG. We do not dispute that for the occasional patient, hairline EEG may reveal the correct diagnosis. However, anecdotal studies and case reports cannot establish the utility of this technique. Indeed, it was our belief that this technique would be adequate for and expedite the diagnosis of NCSE, However, our data has shown otherwise. Bubrick et al. are encouraged to evaluate their data in a prospective manner and publish their results. Emergent EEG is time consuming and not universally available. Though quicker and easier to obtain, hairline EEG does not appear to be an adequate substitute. Further research on this and other alternatives is needed to determine the best method for quickly and accurately determining whether a patient is in NCSE.

PLEDS : corrélations cliniques

We reviewed our experience in 96 consecutive patients exhibiting periodic lateralized epileptiform discharges (PLEDs) on EEG. EEG reports from January 1, 1999 to September 30, 2006 were screened for the term 'PLEDs' and its variants. A retrospective chart review, including examination of neuroimaging and other investigations, was conducted on each patient identified. Acute stroke, tumor and central nervous system infection were the most common etiologies, accounting for 26%, 12% and 12% of cases respectively. Acute hemorrhage and traumatic brain injury combined accounted for another 12%. Previously unreported etiologies included posterior reversible encephalopathy syndrome (PRES), familial hemiplegic migraine and cerebral amyloidosis. There were 9 cases of chronic PLEDs attributable to underlying cortical dysplasia or severe remote cerebral injury, all with an accompanying partial seizure disorder. A prominent role for alcohol withdrawal was noted, and in 6 cases was the sole etiological factor. Fever was present as a potential contributing factor in 40% of cases, and significant metabolic abnormalities in 35%. Seizure activity occurred in 85% of patients overall, but in 100% of patients with PLEDs Plus and BiPLEDs Plus. The overall mortality rate was 27%. Mortality among patients with BiPLEDs however was almost twice that, at 52%. This case series demonstrates the wide variety of potential PLED etiologies. It also emphasizes that despite advances in neurocritical care, the morbidity and mortality associated with PLEDs has changed little since their recognition four decades ago.

Blind Source Separation of Concurrent Disease-Related Patterns from EEG in Creutzfeldt–Jakob Disease for Assisting Early Diagnosis

Creutzfeldt-Jakob disease (CJD) is a rare, transmissible and fatal prion disorder of brain. Typical electroencephalography (EEG) patterns, such as the periodic sharp wave complexes (PSWCs), do not clearly emerge until the middle stage of CJD. To reduce transmission risks and avoid unnecessary treatments, the recognition of the hidden PSWCs forerunners from the contaminated EEG signals in the early stage is imperative. In this study, independent component analysis (ICA) was employed on the raw EEG signals recorded at the first admissions of five patients to segregate the co-occurrence of multiple disease-related features, which were difficult to be detected from the smeared EEG. Clear CJD-related waveforms, i.e., frontal intermittent rhythmical delta activity (FIRDA), fore PSWCs (triphasic waves) and periodic lateralized epileptiform discharges (PLEDs), have been successfully and simultaneously resolved from all patients. The ICA results elucidate the concurrent appearance of FIRDA and PLEDs or triphasic waves within the same EEG epoch, which has not been reported in the previous literature. Results show that ICA is an objective and effective means to extract the disease-related patterns for facilitating the early diagnosis of CJD.

Chronic PLEDs with transitional rhythmic discharges (PLEDs‐plus) in remote stroke

Background. Periodic lateralized epileptiform discharges (PLEDs) are a rare phenomenon in electroencephalography, occurring in acute structural brain lesions. In general, PLEDs appear transiently in acute lesions, but a few reports have described persistent PLEDs in chronic lesions. Case report. An 86-year-old female was admitted, in 1999, with a left MCA stroke associated with right hand focal motor seizures. The first EEG in February of 2002 showed PLEDs over the left hemisphere associated with rhythmic discharges (PLEDs-plus). The patient was admitted on a second occasion in 2003 because of three sequential seizures and the EEG showed a similar pattern. Finally in 2006, the patient was admitted again because of sequential complex partial seizures and an EEG showed the same PLEDS-plus pattern as the EEGs of 2002 and 2003. Discussion. We report an unusual case of chronic PLEDs associated with rhythmic discharges in a patient with recurrent seizures and remote stroke.

Nonconvulsive Seizures in the Pediatric Intensive Care Unit: Out of Sight, Out of Mind?

Nonconvulsive Seizures in the Pediatric Intensive Care Unit: Etiology, EEG, and Brain Imaging Findings. Saengpattrachai M, Sharma R, Hunjan A, Shroff M, Ochi A, Otsubo H, Cortez MA, Carter Snead O III. Epilepsia 2006;47(9):1510–1518. PURPOSE: To determine the occurrence of nonconvulsive seizures (NCS) in the Pediatric Intensive Care Unit (PICU); to ascertain the relationship of NCS to past medical history, etiology, EEG, and brain imaging; and to determine the concordance between abnormal EEG findings and neuroimaging abnormalities. METHODS: A retrospective review was conducted of all pediatric patients who were admitted or transferred to the PICU from January 2000 to December 2003 with an unexplained decrease in level of consciousness, no overt clinical seizures, and EEG recordings performed within the 24 hours of onset of an altered state of consciousness. RESULTS: Twenty-three of 141 patients who met criteria for inclusion in the study (16.3%) were found to have NCS. The male-to-female ratio was 1.9:1. The largest group of patients (43%) had no preexisting neurological condition prior to the onset of NCS. In the remainder, the etiology of NCS included: acute structural brain lesion (48%), acute nonstructural brain lesion (22%), epilepsy-related seizure (13%), and others (17%). Epileptic foci were lateralized to the right side in 39.2%, the left side in 30.4%, and were bilateral in 30.4%. Of 23 patients with NCS, 18 (78.3%) demonstrated abnormal neuroimaging. In 10 of 18 of these patients (55.6%), the findings on neuroimaging were concordant with the lateralization found on EEG ( p &lt; 0.05, Fisher's exact test). CONCLUSIONS: NCS are not uncommon in pediatric patients with an altered state of consciousness. Almost half of the patients were previously healthy especially if they were under 6 months of age. This report highlights the importance of clinical awareness of NCS in the PICU. Nonconvulsive Status Epilepticus in Children: Clinical and EEG Characteristics. Tay SK, Hirsch LJ, Leary L, Jette N, Wittman J, Akman CI. Epilepsia 2006;47(9):1504—1509. BACKGROUND: Nonconvulsive status epilepticus (NCSE) is a highly heterogeneous clinical condition that is understudied in the pediatric population. OBJECTIVE: To analyze the epidemiological, clinical, and electroencephalograpic features in pediatric patients with NCSE. METHODS: We identified 19 pediatric patients with NCSE from the epilepsy database of the Comprehensive Epilepsy Center at Columbia University between June 2000 and December 2003. Continuous EEG monitoring was analyzed and chart review was performed. RESULTS: The patients ranged from 1 month old to 17 years of age. Five patients developed NCSE following convulsive status epilepticus (CSE), and a further 12 patients developed NCSE after brief convulsions. Two developed NCSE as the first manifestation during a comatose state following hypoxic events. Acute hypoxic-ischemic injury was the most frequent etiology of NCSE in our population (5 of 19; 26%), followed by exacerbation of underlying neurometabolic disease (4 of 19; 21%), acute infection (3 of 19; 16%), change in antiepileptic drug regimen (3 of 19; 16%), refractory epilepsy (2 of 19; 11%), and intracranial hemorrhage (2 of 19; 11%). Six patients had associated periodic lateralized epileptiform discharges (PLEDs), one had generalized periodic epileptiform discharges (GPEDs). Five (5 of 19; 26%) patients died of the underlying acute medical illness. Periodic discharges were associated with worse outcome. CONCLUSIONS: The majority of our patients with NCSE had preceding seizures in the acute setting prior to the diagnosis of NCSE, though most of these seizures were brief, isolated convulsions (12 patients) rather than CSE (five patients). Prolonged EEG monitoring to exclude NCSE may be warranted in pediatric patients even after brief convulsive seizures. Prompt recognition and treatment may be necessary to improve neurological outcome.

Assessment of Hairline EEG as a Screening Tool for Nonconvulsive Status Epilepticus

Because of the high incidence of nonconvulsive status epilepticus (NCSE), the attraction of a "quick and easy" screening electroencephalogram (EEG) is obvious. Previous studies have shown utility of hairline EEG in diagnosing epilepsy. However, this technique has not been evaluated as a screening tool for NCSE. We wanted to provide proof of principle that a screening hairline EEG has sufficient sensitivity to use as a screening tool for diagnosing NCSE. A total of 120, 2- to 3-min EEG samples of normal and various abnormal digital EEG studies were reformatted in three six-channel montages (A, longitudinal bipolar; B, referential to ipsilateral ear; C, referential to contralateral ear) that mimicked a hairline recording and were interpreted by five neurophysiologists. The test data interpretation was compared with the original EEG interpretation. Performance was best with montages A and B; 71% and 70.5% of the samples were interpreted correctly by using these montages. Only 65% of the samples were correctly interpreted by using montage C. With the best montage (A), the sensitivities ranged from 91% for normal EEG to 54% for periodic lateralized epileptiform discharges (PLEDs). The sensitivity for seizures was only 72%. Seizures were frequently misinterpreted as more benign patterns such as normal and diffuse slowing. EEG data reformatted to resemble a hairline EEG had low sensitivity for detecting seizures. As a result, we do not recommend further pursuit of hairline EEG as a "quick and easy" screening tool for NCSE.

Neuroimaging and Neurophysiology of Periodic Lateralized Epileptiform Discharges: Observations and Hypotheses

We assessed neuroimaging lesion type and distribution in patients with periodic lateralized epileptiform discharges (PLEDs), with a view to identifying electrographic differences between PLEDs associated with differing lesion locations. Our observations led us to consider a conceptual synthesis between PLEDs and periodic complexes (PCs). Retrospective review of acute neuroimaging results (CT/MRI) on patients identified to have EEG PLEDs, for the period 1999-2003 (n=106). Blinded classification of original EEG recordings. Neuroimaging abnormalities were classified as acute or chronic cortical, or acute or chronic subcortical. Seven out of 106 scans were classified nonlesional. Overall approximately 70% of scans had cortical abnormalities, whether acute or chronic; approximately 23% had subcortical abnormalities. "Cortical" PLEDs were significantly longer in duration (p<0.05) and more variable in morphology (p<0.01) than "subcortical" PLEDs. Structural brain disease commonly, but not invariably, underlies PLEDs; lesion type is spatiotemporally variable. Cortical and subcortical PLEDs have distinct EEG signatures. There is evidence that these may relate to mechanisms for other pathological large-scale oscillatory brain synchronies (e.g., PCs).

Periodic Lateralized Frontal Epileptiform Discharges with Ipsilateral Epilepsia Partialis Continua

Lateralized clonic jerks of the extremities during epileptic seizures usually arise from the contralateral rolandic cortex. In our exceptional case one-sided extremity twitches related to epileptiform activity in the ipsilateral frontal lobe. Case study with clinical-electroencephalographic correlation. A 47-year-old man suffered destruction of most of his right cerebral hemisphere, including the perirolandic region. Epilepsia partialis continua (EPC) ensued, with clonic jerks of the proximal right upper and lower limbs temporally related to periodic lateralized epileptiform discharges (PLEDs) from the parasagittal region of the right frontal lobe with a variable time interval over 100 ms. Sectioning of the subcortical callosal and projection connections of the frontal lobe abolished the clonic jerks. We propose the ipsilateral EPC arose from projections from the supplementary motor region to the medullary reticular formation to account for the long and variable latency between PLEDs and jerks.