Periodic Lateralized Epileptiform Discharges Research Articles

BIPLEDs in akinetic mutism caused by bilateral anterior cerebral artery infarction

Introduction: Akinetic mutism is described as a result of many disorders. Bilateral infarction of the anterior cerebral artery (ACA) territory is reported rarely, however, often leading to akinetic mutism. Case report: We report a 70 year-old man with akinetic mutism due to bilateral ACA infarction. Electroencephalography, 24 h after admission, showed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) in the frontal region and diffuse theta and polymorphic delta activity. Discussion: Postanoxic encephalopathy, central nervous system infection and chronic seizure disorders are the major causes of BIPLEDs. However, BIPLEDs may occur in bilateral ACA territory infarction.

SPECT in periodic lateralized epileptiform discharges (PLEDs): a form of partial status epilepticus?

Periodic lateralized epileptiform discharges (PLEDs) are a well defined electroencephalographic entity but whether PLEDs represent an ictal condition or not remains debated. Much work has been done using electroencephalography (EEG) but new approaches using cerebral perfusion imaging may give more information about this question. We aimed to evaluate if PLEDs were associated with high regional cerebral blood flow (rCBF). We studied 18 patients with PLEDs and different pathologies, and performed brain single-photon-emission computed tomography (SPECT) during and, for three cases, after the disappearance of PLEDs. Qualitative variations and locations of rCBF were compared with PLEDs. Association with seizures and type of seizures were also assessed. SPECT showed high rCBF in 18/18 patients (100%). The location of PLEDs and high rCBF matched in 17/18 cases (94%). In the three cases where SPECT was performed after PLEDs disappeared, the high rCBF had cleared (100%). Eighteen cases (100%) presented seizures before recording of PLEDs, mainly motor (partial motor or generalized tonic–clonic). Where there was a decreased rCBF (related to a lesion) there was little relationship to PLEDs and all patients with decreased rCBF had an adjacent increased rCBF. These results confirm preliminary case reports. Hyperperfusion adds further to the argument that PLEDs may be related to a form of partial status epilepticus.

Periodic lateralized epileptiform discharges after evacuation of subdural hematomas.

Periodic lateralized epileptiform discharges (PLEDs) have been recorded in some patients with subdural hematomas. In most of the patients, PLEDs occurred before the hematoma was evacuated. Five patients (three men and two women) who ranged in age from 57 to 88 years had PLEDs and seizures after evacuation of a subdural hematoma. The PLEDs occurred 1 to 9 days after evacuation and were associated with clinical seizures and altered consciousness. After treatment with anticonvulsant agents, the PLEDs and seizures resolved. The presence of PLEDs should be considered in patients who, after evacuation of a subdural hematoma, have altered consciousness, lateralized neurologic findings, or seizurelike activity (or a combination of these features).

Multifocal periodic lateralized epileptiform discharges (PLEDs): EEG features and clinical correlations

Objective: To analyze the clinical and EEG findings of patients with multifocal periodic lateralized epileptiform discharges (PLEDs). Methods: EEGs containing multifocal PLEDs (3 or more foci of PLEDs) were reviewed. Thirty-five patients (15 males and 20 females), from 2.5 months to 91 years old, met the criteria for multifocal PLEDs. Results: The disease processes identified in the patients included vascular lesions in 9, central nervous system infections in 7, metabolic/toxic disorders in 6, exacerbation of a chronic seizure disorder in 6, hypoxic ischemic insults in 3, and fat embolism, paraneoplastic encephalitis, cerebral metastasis, and multiple sclerosis in one each. Twenty patients died. Detection of the spatiotemporal distribution of multifocal PLEDs was facilitated by the use of Laplacian montages. Conclusions: Multifocal PLEDs were recorded in 35 patients and were associated with processes resulting in diffuse or multifocal cerebral dysfunction. Multifocal PLEDs indicate a significant disturbance of cerebral function and are associated with a mortality rate of 57%.

The clinical significance of periodic lateralized epileptiform discharges in acute ischemic stroke

Objective: To evaluate the incidence and the clinical significance of periodic lateralized epileptiform discharges (PLEDs) in acute ischemic stroke. Methods: Fortyseven consecutive patients with acute ischemic stroke in the anterior circulation who had an electroencephalogram (EEG) within 24 hours of the onset of symptoms were included. A second EEG was performed at 36 ± 12 hours and a third one at 60 ± 12 hours. The functional outcome was assessed at day 90. Results: Overall, we found PLEDs in 13 (27.7%) patients. The first EEG demonstrated PLEDs in 9 patients. Only 1 patient had a seizure. PLEDs were associated with age, early ischemic changes on baseline computed tomography (CT) scan, high mortality, and poor functional outcome. PLEDs on the first EEG were associated with increased risk of early clinical deterioration. Conclusion: PLEDs are common in acute ischemic stroke. In this setting they are not associated with seizures. PLEDs may be a marker of severe brain injury.

Correlation between Clinical Stages and EEG Findings of Subacute Sclerosing Panencephalitis

In this retrospective study 67 patients with SSPE seen between the years 1980 and 1998 were reviewed. Using the criteria of SSPE diagnosis (clinical signs, characteristic EEG patterns, high titres of measles antibodies in the serum and CSF), the patients were divided into two groups. Group A fulfilled all criteria, however, due to the inability of measuring measles antibody before 1987, it was not possible to observe the third criterion in Group B. Among 67 patients, groups A and B consisted of 51 boys and 16 girls ranging in age between 1 to 23 years, mean age 13.1. The male/female ratio was 3.1. The periodic EEG complexes (PCs) were usually bilateral, synchronous and symmetrical. PC amplitude asymmetry was seen in 12 patients and 2 patients had no PC synchronization between the hemispheres. Six patients had more than one form of PC. Delta activity in anterior hemispheres after PC was seen in 40 patients, mostly in stage 2A. Thirty-two patients had focal epileptiform abnormalities in multiple locations at every stage but most frequently in frontal, central and temporal regions. One patient had PC over both hemispheres and periodic lateralized epileptiform discharges (PLEDs) over the right hemisphere. The EEG findings described and observed in our study do not seem to be specific to SSPE but these findings were not atypical or unusual.

Periodic lateralized epileptiform discharges: association with seizures

The clinical features and EEGs of 45 consecutive patients (40 adults and 5 children) who had periodic lateralized epileptiform discharges (PLEDs) were reviewed to determine the relationship between seizures and PLEDs. Focal encephalitis and ischemic stroke were the most frequent underlying processes for adult patients . All of the children, but only six of the adults, had long-lasting cerebral disorders whereas the remaining adults had acute or subacute illness. There were 38 patients (84.4%) experiencing a seizure disorder. Twenty-six of them had their first seizure during their acute illness, as the pattern of PLED was encountered. Eight cases had status epilepticus, and seven of them had epilepsia partialis continua. Nineteen patients had a recent seizure in the day when PLEDs were observed but not during EEG recording; 12 patients had their seizures within 10 days before the observation of PLED. PLEDs were grouped into three categories with respect to their extensions: lateralized to one hemisphere (n= 22), localized in one region (n= 17) and being prominent over one side with contralateral spread (n= 6). The last group was found to be more closely associated with frequent seizures or status epilepticus than the other two groups. Our results showed that PLEDs were highly correlated with recent seizures in the majority of the patients. These EEG findings may be considered as a manifestation of an increased neuronal excitability caused by different etiologies; but not an ictal pattern.

BIPLEDs with Complete and Rapid Recovery in a Patient with AIDS Encephalopathy

ABSTRACT.A 33-year-old male with AIDS (CD4=12), dementia, spasticity, and MRI findings of cerebral atrophy and deep white matter changes was admitted for the treatment of chronic cough and cellulitis of the legs. Two days after admission, the patient exhibited the first seizure of his life—a generalized convulsion lasting five minutes. An EEG obtained 14 hours after the convulsion revealed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) with prominent asynchrony. CT and MRI showed abnormalities similar to those present one year before. CSF studies obtained the day after the seizure were normal. The only medication started in the hospital prior to the onset of the seizure was intravenous nafcillin. Immediately after the seizure, nafcillin was discontinued and a loading dose of 1500 mg PE of fosphenytoin was given followed by oral maintenance. Another EEG, three days later, demonstrated the complete resolution of BIPLEDs. No other seizures occurred. With antibiotic therapy the cellulitis and pneumonia resolved and, within two weeks, the patient was discharged home on phenytoin. We propose that in patients with AIDS encephalopathy, the occurrence of coma, seizures, and BIPLEDs should not be assumed to be a poor prognostic sign.

Sclérose en plaques et état de mal épileptique partiel non convulsif

Partial non-convulsive status epilepsy in multiple sclerosis. This report describes the observations of two patients with a several years' history of multiple sclerosis who presented sudden neurologic impairment. The symptomatology was suggestive of a non-convulsive partial status epilepsy. The clinical presentation was a paroxysmal dysphasic phenomenon in the first case without any consciousness impairment, associated with slight right hemiparesis. Electroencephalographic investigations revealed asymmetrical patterns, left-sided slow waves and periodic lateralized epileptiform discharges (PLEDs). Antiepileptic treatments were partially effective and intravenous steroids were needed for complete recovery. For the second patient, clinical presentation was acute psychiatric symptoms with disorientation, alternating manic symptomatology and mutism. Electroencephalography showed left fronto-central rhythmic continuous slow wave and spike wave activity. Intravenous antiepileptic treatment quickly improved the symptomatology. These observations draw attention to the fact that an epileptic cause should not be ruled out when a patient with multiple sclerosis presents sudden neurologic or psychiatric impairment. An early diagnosis allows immediate antiepileptic treatement. Intravenous steroids can be added to stop seizures.

Magnetoencephalographic analysis of periodic lateralized epileptiform discharges (PLEDs)

Objective: To clarify the spatial and temporal distribution of the electroencephalographic (EEG) pattern termed ‘periodic lateralized epileptiform discharges’ (PLEDs), we performed magnetoencephalography (MEG) to analyze PLEDs in a patient with a right parietal metastasis associated with meningeal carcinomatosis.Methods: A 37-channel biomagnetometer was used to simultaneously record the EEG and MEG. Equivalent current dipole (ECD) source localization was calculated based on a single-dipole model and mapped onto a magnetic resonance image. Single-photon emission computed tomography with technetium-99-hexamethyl-propyleneamine oxime (HMPAO-SPECT study) was also performed during both presence and absence of PLEDs according to an EEG monitor.Results: By EEG the PLEDs, predominantly right-sided, consisted of a typical negative triphasic spike followed by a slow negative wave. By MEG the PLEDs had a sequence with 3 distinct components. ECDs in the 3 components were localized to the cortex around the lesion, although exact localization and dipole direction varied between components. HMPAO-SPECT demonstrated hypoperfusion of the lesion and adjacent cortex during both quiescence and appearance of PLEDs.Conclusion: Our results indicate that PLEDs originated from the hypoperfused cortex surrounding the lesion.

The periodicity of lateralized epileptiform discharges

Objectives: Although the term periodic lateralized epileptiform discharges (PLEDs) was introduced in 1964, there has been little discussion about the definition of periodicity, whether the degree of periodicity has clinical significance, and whether electroencephalographers can accurately assess periodicity. The objectives of this study were to determine if a mathematical descriptor of periodicity could analyse PLEDs and whether such has clinical relevance, to correlate the degree of periodicity with underlying etiology and to assess the accuracy of sight recognition of periodically occurring EEG events.Methods: A 6 year retrospective analysis of EEGs on patients with PLEDs was undertaken. The coefficient of variation of inter-complex intervals was calculated for all records. The relative periodicity of each record was rated by electroencephalographers. Corresponding hospital records were reviewed with regard to clinical and pathological information.Results: In cases of acute viral encephalitis, discharges were more periodic than in other etiologies (P=0.013). Age, clinical state, and time of last seizure did not influence periodicity but 40 (70%) of 57 recordings with PLEDs were done within 2 days of a seizure. A history of seizures was present in 42 (89%) of 47 patients. Electroencephalographers’ assessment of periodicity correlated well with measured periodicity (r=−0.49, P=0.0001). However, EEGers were more likely to assess records as periodic if: discharges occurred frequently (r=−0.48, P=0.0001), or the complexes were visually assessed to have a uniform morphology (r=0.31, P=0.02), even though neither of these factors influenced the periodicity of discharges.Conclusions: PLEDs were objectively measured to be more periodic when they were associated with acute viral encephalitis than with other etiologies. Nonetheless, the considerable overlap of values among the several presenting disorders diminished specificity. Electroencephalographers were able to recognize periodically occurring discharges. However, they were strongly influenced by discharge frequency and their perception of the uniformity of discharge morphology.

Chronic periodic lateralized epileptiform discharges during sleep in a patient with caudate nucleus atrophy: insights into the anatomical circuitry of PLEDs

Objective: Periodic lateralized epileptiform discharges have been recognized for 33 years; however, little is known about the underlying mechanism causing periodic discharges. The following case provides an opportunity to study PLEDs in a patient with precisely localized subcortical grey matter lesions. Methods: Routine EEGs and overnight polysomnography were performed on the study patient. Standard 10–20 electrode positions were used, as well as EOG and chin EMG for polysomnography. Results: The study patient was a 39-year-old woman with severe left caudate nucleus atrophy and right hemi-dystonia. She had left ventral-lateral (VL) thalamotomies in 1989 and 1991, pallidotomy in 1992, and centromedian thalamic stimulator implantation in 1997. EEGs prior to surgical intervention demonstrated left hemisphere PLEDs during sleep. Following CM nucleus stimulatory implantation, the patient had overnight polsomnography. EEG during wakefulness and REM sleep was normal. With stages I–IV sleep left hemisphere PLEDs at 1–2 Hz were seen with fronto-temporal predominance. Sleep spindles were present bilaterally. There was no history of seizures, before or after surgery. Conclusions: The finding of PLEDs confined to synchronized sleep which were not affected by surgical manipulation of the motor basal ganglia circuit suggests a role of the associative basal ganglia circuit in the generation of periodic phenomenon.

Persistent Nonconvulsive Status Epilepticus After the Control of Convulsive Status Epilepticus

Convulsive status epilepticus (CSE) is a major medical and neurological emergency that is associated with significant morbidity and mortality. Despite this high morbidity and mortality, most acute care facilities in the United States cannot evaluate patients with EEG monitoring during or immediately after SE. The present study was initiated to determine whether control of CSE by standard treatment protocols was sufficient to terminate electrographic seizures. One hundred sixty-four prospective patients were evaluated at the Medical College of Virginia/VCU Status Epilepticus Program. Continuous EEG monitoring was performed for a minimum of 24 h after clinical control of CSE. SE and seizure types were defined as described previously. A standardized data form entry system was compiled for each patient and used to evaluate the data collected. After CSE was controlled, continuous EEG monitoring demonstrated that 52% of the patients had no after-SE ictal discharges (ASIDS) and manifested EEG patterns of generalized slowing, attenuation, periodic lateralizing epileptiform discharges (PLEDS), focal slowing, and/or burst suppression. The remaining 48% demonstrated persistent electrographic seizures. More than 14% of the patients manifested nonconvulsive SE (NCSE) predominantly of the complex partial NCSE seizure (CPS) type (2). These patients were comatose and showed no overt clinical signs of convulsive activity. Clinical detection of NCSE in these patients would not have been possible with routine neurological evaluations without use of EEG monitoring. The clinical presentation, mortality, morbidity, and demographic information on this population are reported. Our results demonstrate that EEG monitoring after treatment of CSE is essential to recognition of persistent electrographic seizures and NCSE unresponsive to routine therapeutic management of CSE. These findings also suggest that EEG monitoring immediately after control of CSE is an important diagnostic test to guide treatment plans and to evaluate prognosis in the management of SE.

The "Mozart effect" on epileptiform activity.

The "Mozart Effect," using the Piano Sonata in D Major (K.448), was examined in patients with seizures. In 23 of 29 instances significant decreases in epileptiform activity were noted from patients even in coma, with status epilepticus or with periodic lateralized epileptiform discharges (PLEDs). The effect may be immediate or require 40-300 sec to manifest itself. The change in the amount of ictal activity in one patient in coma was from 62% before the music to 21% during Mozart. Amplitudes of these discharges also have often decreased. Examples of PLEDs on both temporal areas are shown in which the effect was only on the left temporal area but in other patients only on the right temporal area. Brain maps during the music showed theta and alpha activity decreased on the central areas, while delta waves increased on the frontal midline area. The basis of this effect is likely that the superorganization of the cerebral cortex with its highly structured radial columns seen throughout both hemispheres may resonate with the superior architecture of Mozart's music.

Polymerase chain reaction-proved herpes simplex encephalitis in children.

To investigate the clinical features in PCR-proved herpes simplex encephalitis (HSE) in children, excluding neonates. We studied the clinical manifestations and laboratory findings of 24 children in whom the diagnosis of herpes infection was confirmed by the PCR assay and compared them with those of 38 children with central nervous system infections other than HSE. There were no significant differences between groups in the percentage with fever or convulsions, the initial neurologic symptoms or the level of consciousness. Analysis of cerebrospinal fluid showed no significant differences in the cell count or concentration of protein and glucose. Computerized tomography of the brain identified localized abnormalities in 18 (75%) of the 24 HSE patients and in 10 (31%) of the 32 non-HSE patients (P = 0.001). Periodic lateralized epileptiform discharges, abnormal findings on electroencephalography, were detected in 8 (36%) of 22 HSE patients and in none of the non-HSE patients (P = 0.0001). The rates of moderate to severe morbidity and death were significantly higher in the HSE patients than in the non-HSE patients. Of the 9 HSE patients with a Glasgow Coma Scale score > or = 11, all patients recovered completely. HSE patients younger than 3 years of age were more likely to develop severe sequelae or to die of the disorder than older patients (P = 0.02). There were no specific clinical characteristics of HSE patients. The results of electroencephalography and computerized tomography were helpful, but not confirmatory, in diagnosing HSE. The Glasgow Coma Scale score and age significantly influenced the mortality and morbidity in the HSE patients.

Periodic epileptiform discharges in the midline.

Five patients had electroencephalograms (EEGs) that showed periodic epileptiform discharges in the midline (PEDIM); other than location, this activity has the same characteristics as periodic lateralized epileptiform discharges (PLEDs). All 5 patients had acute onset of partial motor seizures involving the lower extremity. The location of the PEDIM corresponded to the seizure type and focal neurologic deficits. All 5 patients had sustained a cerebrovascular insult, either old or new, and the PEDIM and seizures suggested an origin from the watershed area between the anterior, middle, and posterior cerebral arteries, involving predominantly the parasagittal region of the cerebral hemisphere.

Periodic lateralized epileptiform discharges in mitochondrial encephalomyopathy

Periodic lateralized epileptiform discharges (PLEDs) were transiently recorded during the acute phase of cerebral stroke-like episodes in three patients with mitochondrial encephalomyopathy (MEM). One of the patients developed stroke-like episodes three times, always accompanied by PLEDs. These discharges were recorded from the hemisphere responsible for the stroke-like episodes or from the more severely affected hemisphere when bilateral hemispheres were affected. Although PLEDs have been rarely reported in MEM, this disease should be considered as a differential diagnosis of cerebral infarction with PLEDs.

Aphasia, partial seizures, and regional epileptiform EEG changes

The relationship of epileptiform activity to episodes of aphasia requires definitive clinical-electroencephalogram (EEG) study. We present a case series of seven right-handed patients with adult-onset, recurrent language disturbance in association with seizures or EEG epileptiform activity. The left posterior speech or nearby association area(s) was involved in each case. In two patients the anterior speech area was probably also affected. On EEG, seizures, periodic lateralized epileptiform discharges (PLEDs) or PLEDs plus patterns were found in the left hemisphere, most commonly in the temporoparietal regions. Etiologies were: cavernous hemangioma (two patients), trauma (two patients), hemorrhage from congophilic angiopathy (one patient), ischemic stroke (one patient), and undetermined (one patient). Localization of lesions: left parietooccipital (one patient), left posterotemporal (one patient), left midtemporal region (one patient), left hippocampal gyrus (one patient), and poorly localized in left cerebral convexity (three patients). Differentiation from nonepileptiform mechanisms was possible using scalp EEG and clinical criteria.

2-17-20 Imaging studies in patients with periodic lateralized epileptiform discharges

2-17-20 Imaging studies in patients with periodic lateralized epileptiform discharges

Periodic lateralized epileptiform discharges (PLEDs) following stroke are associated with metabolic abnormalities

PLEDs are an electroencephalographic phenomenon consisting of high voltage stereotyped periodic transients distributed over one hemisphere, associated with acute or subacute structural lesions as well as with metabolic abnormalities. We have evaluated the contribution of metabolic factors in patients with acute hemispheric stroke. Temperature, serum electrolytes, glucose, kidney and liver function tests were examined in two groups of 14 patients each following acute hemispheric stroke differing in regard to the appearance of PLEDs in the EEG. CT features of the infarcts were also compared. Patients with PLEDs had more metabolic derangements as compared to patients with no PLEDs (mann-Whitney ranking test P = 0.01). Hyperglycemia and fever were significantly associated with PLEDs (logistic regression model, P < 0.05). There was no significant difference regarding radiological findings between the two groups. We conclude that acute stroke as a structural lesion predisposes to PLEDs but the latter may be triggered by metabolic disturbances, mainly hyperglycemia and fever.