Periodic Lateralized Epileptiform Discharges Can Survive Anesthesia

Neurology International 2017; volume 9:6933

Periodic lateralized epileptiform discharges Introduction Correspondence: Edward C. Mader Jr., Department of Neurology, Louisiana State can survive anesthesia Pathological activation of a cortical University Health Sciences Center, 1542 and result in asymmetric region at a rate of about 1/s can be detected Tulane Ave Rm 111B, New Orleans, LA in the electroencephalogram (EEG) as peri- 70112, USA. drug-induced odic lateralized epileptiform discharges E-mail: [email protected] burst suppression (PLEDs), a term introduced by Chatrian et al. in 1964.1 PLEDs consist of periodic sharp Key words: PLEDs; Burst suppression; Seizure; Anesthesia; Propofol. Edward C. Mader Jr., waves, slow waves, and/or multiwave com- Louis A. Cannizzaro, Frank J. Williams, plexes that are lateralized, i.e. electrodes near the cortical generator on one side of the Disclosure: the authors were not directly Saurabh Lalan, Piotr W. Olejniczak involved with the care and management of the head record the highest voltage while elec- Department of Neurology, Louisiana patient. Their role was limited to EEG moni- trodes distant from the generator on the con- toring and interpretation. State University Health Sciences Center, tralateral side may or may not pick up some 1,2 New Orleans, LA, USA of the volume conducted signal. When two Conflict of interest: the authors declare no cortical foci, one in each hemisphere, gener- potential conflict of interest. ate PLEDs independently, the pattern is referred to as bilateral independent PLEDs Acknowledgments: we are grateful to our Abstract (BiPLEDs).3 Two PLEDs-generating foci EEG technologists Thomas Miller, Sheryl may also be in the same hemisphere.4 Other Wagamonte, and Lisa Keppard for recording Drug-induced burst suppression (DIBS) less familiar variants include three or more high-quality electroencephalograms. is bihemispheric and bisymmetric in adults PLEDs-generating foci,5,6 PLEDs with max- and older children. However, asymmetric Received for publication: 13 October 2016. imum voltage in the midline,7 and alternating DIBS may occur if a pathological process is Accepted for publication: 9 January 2017. PLEDs.8 Most PLEDs occur in patients with affecting one hemisphere only or both acute focal destructive brain lesions (e.g. only hemispheres disproportionately. The usual This work is licensed under a Creative stroke, herpes encephalitis, traumatic brain Commons Attribution NonCommercial 4.0 suspect is a destructive lesion; an irritative injury), chronic brain lesions (e.g. tumors, License (CC BY-NC 4.0). or epileptogenic lesion is usually not inflammatory lesions), and epilepsy (with or invoked to explain DIBS asymmetry. We without discrete lesions).9-13 PLEDsuse and ©Copyright E.C. Mader Jr et al., 2017 report the case of a 66-year-old woman with Licensee PAGEPress, Italy BiPLEDs have also been reported in a vari- new-onset seizures who was found to have Neurology International 2017; 9:6933 a hemorrhagic cavernoma and periodic lat- ety of toxic and metabolic encephalopathies, doi:10.4081/ni.2017.6933 eralized epileptiform discharges (PLEDs) in encephalitides, and neurodegenerative 2,3,9-13 the right temporal region. After levetirac- processes. etam and before anesthetic antiepileptic PLEDs are considered epileptiform nomena. PLEDs are resistant to treatment 22 drugs (AEDs) were administered, the elec- because patients with PLEDs have a high with antiepileptic drugs (AEDs). In this troencephalogram (EEG) showed continu- probability of experiencing seizures; in regard, PLEDs resemble focal interictal ous PLEDs over the right hemisphere with some series the probability is about 50- spikes more than seizures. It may very well 12-14 maximum voltage in the posterior temporal 100%. Reiher et al. reported a higher be the case that PLEDs represent neuro- region. Focal electrographic seizures also incidence of seizures when PLEDs are physiological processes that are distributed 13 occurred occasionally in the same location. commercialaccompanied by low-voltage fast rhythms along an interictal-ictal continuum. The Propofol resulted in bihemispheric, but not (PLEDs-plus) than when they are not underlying brain injury, preexisting seizure 15 in bisymmetric, DIBS. Remnants or frag- (PLEDs-proper). However, Chong et al. propensity, and coexisting acute metabolic ments of PLEDs that survived anesthesia found that PLEDs-proper rarely occur in derangements determine whether a patient increased the amplitude and complexity of isolation and that the EEG often fluctuates develops interictal PLEDs, ictal PLEDs, 16 the bursts in the right hemisphereNon leading to between PLEDs-proper and PLEDs-plus. electrographic seizures, or a combination of 16 asymmetric DIBS. Phenytoin, lacosamide, It has been debated for decades whether these patterns. Some authors have pro- ketamine, midazolam, and topiramate were PLEDs are ictal or interictal. Those who posed a treatment algorithm for PLEDs and administered at various times in the course argue that PLEDs are ictal point to the clin- other EEG patterns based on the theory of of EEG monitoring, resulting in suppres- ical correlates of PLEDs, such as motor, an interictal-ictal continuum.23,24 sion of seizures but not of PLEDs. sensory, and cognitive changes,17 or to the There is also evidence that PLEDs are Ketamine and midazolam reduced the rate, presence of focal glucose hypermetabolism not always epileptiform. Gross et al report- amplitude, and complexity of PLEDs but on positron emission tomography (PET)18 ed chronic PLEDs during sleep in a patient only after producing substantial attenuation and focal hyperperfusion on single-photon with ipsilateral caudate nucleus atrophy25 of all burst components. When all anesthet- emission computed tomography and Wheless et al reported PLEDs in a ics were discontinued, the EEG reverted to (SPECT),19 not to mention the resolution of patient with acute thalamic stroke.26 the original preanesthesia pattern with con- these findings when PLEDs disappear. Because the presence of an underlying tinuous non-fragmented PLEDs. The fact Nonetheless, some studies have shown that epileptic disturbance and the risk of neu- that PLEDs can survive anesthesia and focal hypermetabolism and/or hyperperfu- ronal injury are still unknown in some peri- affect DIBS symmetry is a testament to the sion may also occur during focal interictal odic and rhythmic EEG patterns (PLEDs robustness of the neurodynamic processes spikes.20,21 Electrographic seizures may included), the American Clinical underlying PLEDs. emerge during PLEDs, coexist with PLEDs, Neurophysiology Society (ACNS) adopted or evolve on top of PLEDs10,14 suggesting a nomenclature for rhythmic and periodic that seizures and PLEDs are distinct phe- EEG patterns, first published in 200527 and

[Neurology International 2017; 9:6933] [page 1] Case Report updated in 2012.28 The goal was to have a gency department (ED) and was treated care unit (ICU). On admission, her vital standard terminology for research and with lorazepam 4-mg IV and levetiracetam signs, oxygen saturation, blood cell counts, expert communication. Terms with clinico- 1500-mg IV load/750-mg q12. Her past glucose, electrolytes, liver and kidney func- pathologic undertones, such as triphasic medical history was significant for diabetes tion tests, urinalysis, and toxicology were waves and epileptiform, were discouraged mellitus and hypertension but negative for all within normal limits. in favor of terms that are more descriptive seizure or epilepsy. The patient remained Head CT was performed in the ED, fol- of the EEG pattern and that are non-com- stuporous and was admitted to the intensive lowed 12 h later by a magnetic resonance mittal with respect to pathophysiology. Thus, the new term lateralized periodic discharges or LPDs is preferred to the old term PLEDs. ACNS is not necessarily suggesting that we completely abandon all of the old terms for clinical use.27,28 In this paper, we will continue using the old and familiar term PLEDs. Burst suppression was initially observed as a response of the EEG to high doses of anesthetic agents.29 Like PLEDs, drug-induced burst suppression (DIBS) is periodic with bursts of high-voltage activity alternating with periods of severe background attenuation or suppression.29,30 The cortical discharges in DIBS are clustered into bursts with variable amounts of slow waves, fast waves, and sharp waves (usually higher in amplitude than PLEDs) and the only periods of suppression are characterized by isoelectric or severely attenuated EEG (usually more attenuated than the background in PLEDs).30 DIBS is used to monitor the use effectiveness of anesthetic AEDs during treatment of refractory status epilepticus.31,32 The presence of DIBS in the EEG is often equated with adequate suppression of epileptic activity, including ictal and interictal PLEDs. However, whether DIBS is appropriate for all cases of status epilepticus and the duration and interburst interval of DIBS that is optimal for suppressing epileptic activity without causing hypoten- sion and other anesthesia-related morbidi- ties remains unknown.31-34 commercial We report a case [note that the authors were involved with EEG monitoring but not with the clinical management of the patient] wherein PLEDs survived treatment with multiple AEDs, including three anestheticsNon (propofol, ketamine, and midazolam), and persisted during DIBS in the form of PLEDs remnants or fragments that resulted Figure 1. Brain structural imaging showing a circumscribed lesion in the inferior aspect in DIBS asymmetry. The PLEDs reverted of the right temporal lobe. Non-contrast CT (CT) shows a punctate hyperintensity in the right temporal area suggestive of calcification. The magnetic resonance imaging (MRI) back to the original continuous (not frag- signal characteristics of the lesion are consistent with a cavernous malformation or cav- mented) preanesthesia EEG pattern after ernoma with late subacute hemorrhage (core) and old chronic hemorrhage (rim) corre- withdrawal of anesthesia. sponding to a type I cavernoma in the MRI-based classification of Zabramski et al.35 The lesion is hyperintense (bright) on diffusion-weighted imaging (DWI) with high apparent diffusion coefficient (ADC) in the core and low ADC in a portion of the rim. The core is hyperintense on T1-weighted (T1a, T1c) and T2-weighted (T2a, T2c) images, indicating extracellular methemoglobin deposits from late subacute hemorrhage (age of 1 to 4 Case Report weeks). The rim is isointense on T1a, slightly hypointense on T1c, and moderately hypointense on T2-weighted sequences. On gradient echo sequences (GRE1), the bright A 66-year-old woman was found wan- lesion core is surrounded by a very dark rim (blooming artifact), indicating peripheral dering aimlessly on the street with bruises deposits of hemosiderin (a paramagnetic compound) from an old hemorrhage (age>1 on the extremities. Emergency responders month). Peripheral calcium deposits may also account for some of the blooming since suspected that she had an unwitnessed con- hyperintensity was present on CT (see above). GRE sequences (GRE2) also revealed addi- tional lesions with hypointense (dark) spots in other brain locations, which may repre- vulsion and was in a postictal state. She had sent multiple asymptomatic hemorrhages in the past, perhaps from other cavernomas. a tonic-clonic seizure while in the emer-

[page 2] [Neurology International 2017; 9:6933] Case Report imaging (MRI) scan of the brain (Figure 1). antiepileptic therapy. Phenytoin 1300-mg plexity of DIBS decreased, and most fast Contrast was not used in both studies. CT IV load/100-mg IV q8 and lacosamide 200- rhythms disappeared, but PLEDs remnants showed subtle punctate hyperintensity in mg IV load/100-mg IV q12 were added. and DIBS asymmetry persisted (Figure 2C). the right temporal region (Figure 1CT). Ketamine 25 mcg/kg/minute IV was also The addition of midazolam up to 1.2 MRI revealed a well-circumscribed lesion started and incrementally titrated to 65 mcg/kg/minute IV and topiramate 200-mg in the inferior aspect of the right temporal mcg/kg/minute. Electrographic seizures per NGT q12 reduced the burst rate, ampli- lobe with the signal characteristics of a cav- ceased, the burst rate, amplitude, and com- tude, and complexity of DIBS further. ernous malformation or cavernoma, i.e. the lesion consisted of a core of extracellular methemoglobin indicating late subacute hemorrhage (age 1-4 weeks) and a rim of hemosiderin indicating old hemorrhage (age >1 month). Diffusion-weighted imaging (DWI) revealed a hyperintense lesion (Figure 1DWI). The apparent diffusion coefficient (ADC) of the core was high and a portion of the rim had low ADC (Figure 1- ADC). The core was hyperintense on T1- weighted (Figure 1T1a,c) and T2-weighted (Figure 1-T2a,c) images. The rim was isointense or slightly hypointense on T1-weighted (Figure 1T1a,c) and hypointense on T2- weighted (Figure 1T2a,c) images. These signal characteristics correspond to a type I cavernoma in the MRI-based classification only of Zabramski et al.35 Pathologically, a type I cavernoma consists of a center with subacute hemorrhage surrounded by a rim of hemosiderin-stained macrophages and glio- sis.35 MRI gradient echo (GRE) sequences use showed a very dark rim around the bright core, consistent with blooming artifact (Figure 1GRE1). In addition to the main lesion, GRE revealed small asymptomatic hemorrhages near the midline and in the left hemisphere (Figure 1GRE2). These old hemorrhages could have been caused by cavernomas or other vascular lesions that bled in the past. Continuous EEG monitoring was performed over a five-day stretch (Figure 2). After levetiracetam was loaded, but before commercial anesthetic AEDs were administered, the EEG showed PLEDs in the right hemisphere with maximum voltage in the right posterior temporal electrode (P8)Non and rarely Figure 2. Electroencephalogram (EEG) tracings represent different time points (A-E) dur- in the right mid-temporal (T8) or anterior ing treatment with antiepileptic and anesthetic drugs. Display settings: 16-channel lon- gitudinal bipolar montage; filters at 1-Hz high-pass, 70-Hz low-pass, 60-Hz notch; sen- temporal (F8) electrodes (Figure 2A). The sitivity at 7µV/cm; voltage-time scale: 100 µV/1 sec for the full tracings and 50 µV/1 sec PLEDs were not associated with motor or for the magnified epochs. The EEG is shown on the left as a 16-channel trace with the behavioral change. Propofol was started at channels separated from top to bottom into the following groups: left temporal, left 50 mcg/kg/minute IV and DIBS with 5-10 parasagittal, right parasagittal, and right temporal. For clarity, the final 6 seconds of each bursts/minute was achieved with an infu- tracing are magnified and displayed as two 8-channel traces: parasagittal (left over right) derivations in the middle column and temporal (left over right) derivations in the right sion rate of 60 mcg/kg/minute. PLEDs sur- column. A) After levetiracetam was loaded, but before infusion of anesthetic antiepileptic vived as remnants or fragments mixed with drugs, periodic lateralized epileptiform discharges (PLEDs) were present on the right and other burst components or as discharges maximum in the right posterior temporal region. B) Propofol resulted in asymmetric outside the bursts in the interburst intervals drug-induced burst suppression with surviving remnants or fragments of PLEDs on the (Figure 2B). Surviving PLEDs remnants right that are mixed with other burst components increasing the overall amplitude and complexity of bursts on the right. C) The addition of phenytoin, lacosamide, and keta- gave DIBS an asymmetric appearance. The mine reduced the rate and complexity of bursts and caused fast rhythms to disappear but EEG also showed recurrent focal electro- failed to completely suppress the PLEDs remnants. D) The addition of midazolam and graphic seizures arising from the same topiramate resulted in further reduction of burst rate and complexity and attenuation of PLEDs focus (not shown in the figure). The burst components. The PLEDs remnants were also attenuated but not completely sup- tenacity of PLEDs to propofol and the occa- pressed. E) After withdrawal of anesthesia, the PLEDs started to reacquire their preanesthesia configuration. The post-anesthesia trace in this figure shows continuous PLEDs sional occurrence of electrographic seizures with interdischarge interval of 2-3 sec. motivated her physicians to escalate

[Neurology International 2017; 9:6933] [page 3] Case Report

PLEDs remnants were attenuated but did Gloor et al. suggested a form of cortical- case, they considered their findings consis- not disappear (Figure 2D). subcortical interaction in which subcortical tent with the prevailing view that focal By day 5, all anesthetic AEDs have discharges are projected to the cortex and IEDs are not influenced by chronic AED been discontinued and the patient passed cortical recovery time determines discharge therapy in patients with focal epilepsy. the extubation test. Approximately 12 h rate (~1/s).37 Raroque et al. reviewed the There are few reports of successful control after all anesthetic agents were discontin- CT/MRI of 39 patients with of PLEDs using carbamazepine, midazo- ued, the same PLEDs started appearing in PLEDs/BiPLEDs and concluded that struc- lam, pentobarbital, sodium valproate, and the same location (Figure 2E). At first, the tural lesions have a primary role in the felbamate,22 but these studies must be repli- PLEDs were very fragmented and far apart pathogenesis of PLEDs but a role for meta- cated. While the resolution (or progression) with an interdischarge interval >3 s and bolic abnormalities cannot be excluded.38 of the underlying pathology (not the direct minimal periodicity. With time, the PLEDs Brain lesions in patients with PLEDs vary effects of AEDs) is most likely the reason became more continuous and exhibited a in their age and location; however, the PLEDs disappear, most experts still recom- more stable interdischarge interval of 2-3 majority are acute structural lesions in the mend using nonanesthetic AEDs to sec. EEG monitoring was discontinued at cortical gray and the adjacent white mat- decrease the probability of seizures in this point. The patient was successfully ter.39 It is also a fact that some patients with patients with PLEDs. extubated but her clinical course was regret- PLEDs have no CT/MRI evidence of a When anesthetics are administered to tably complicated with metabolic distur- causative brain lesion.9-11 PLEDs may be treat status epilepticus, it is often recom- bances and cardiac arrhythmias: she expired triggered by systemic conditions that lower mended to titrate the anesthetic to achieve a after 9 days in the ICU. the seizure threshold.12,15 Some authors DIBS interburst interval of 2-20 s over a hypothesized that PLEDs are the expression period of 24-48 h.51 However, a recent of a change in excitatory neurotransmission study where a cohort of 19 patients received due to an acute brain lesion producing par- anesthetics for refractory status epilepticus, Discussion tial functional denervation in a localized showed that treatment success was not 8 This case shows that PLEDs can sur- area of the cortex. Studies of EEG phase influenced by the interburst interval or the 52 vive anesthesia and result in asymmetric reversals suggest that PLEDs originate in durationonly of DIBS. In the case presented, DIBS. In general, DIBS asymmetry is hyperexcitable cortex at the margins of the focal electrographic seizures ceased com- 40 attributed to a loss of function, i.e. burst lesion. pletely during DIBS but PLEDs persisted components are attenuated in one hemi- Serial EEG recordings have shown that despite uptitration of anesthetic dosage sphere due to a destructive lesion. An irrita- PLEDs often disappear spontaneously in 2 (propofol up to 60 µg/kg/m, ketamine up to 14,15 use tive or epileptogenic lesion resulting in a to 3 weeks. There are however reports 65 µg/kg/m, and midazolam up to 1.2 41 gain of function in one hemisphere is not of PLEDs persisting for months or years µg/kg/m) to maintain a DIBS interburst 42 usually invoked to explain DIBS asymme- or resolving within a few days of onset. interval of 6-12 s (burst rate of 5-10/m). The try. The patient developed PLEDs second- BiPLEDs tend to be more transitory surviving PLEDs remnants were mixed ary to a hemorrhagic cavernoma in the right because they are triggered by pathological with burst components, occasionally temporal lobe (Figure 1). During DIBS, the processes that progress relentlessly, with spilling over the interburst intervals (Figure PLEDs persisted as PLEDs fragments that other abnormal EEG patterns replacing 2B-D). The original pre-anesthesia pattern were mixed with the burst components of BiPLEDs, or by physiological disturbances of continuous PLEDs (Figure 2A) was DIBS in the right hemisphere (Figure 2). that are highly reversible, e.g. BIPLEDs restored when anesthesia was discontinued The waveform morphology, polarity, and appeared with nafcillin treatment and disap- (Figure 2E). Fishman and Legatt reported a spatial distribution (maximum voltage was peared three days after the drug was discon- case wherein PLEDs were resistant, not often at P8 and occasionally at T8 or F8) tinued.commercial43 Even though PLEDs and BiPLEDs only to AEDs, but also to hypoxia.53 In the indicate that these burst-embedded frag- are self-limited, they are often resistant to course of progressive cerebral dysfunction, ments are the remnants of PLEDs that were treatment with AEDs if the causative patho- the patient’s brain continued producing originally present in the EEG prior to anes- logical processes are still active. In terms of PLEDs until the last minutes of her life; the thesia. These PLEDs remnants increased AED resistance, PLEDs tend to surpass PLEDs disappeared only 40 seconds before the overall amplitude and complexityNon of seizures and resemble focal IEDs. In-vitro the EEG turned isoelectric. The resistance bursts in the right hemisphere giving DIBS experiments showed that AEDs abolish pro- of PLEDs to AEDs, anesthesia, and hypoxia an asymmetric appearance. longed seizure-like discharges at concentra- reminds us of the robustness of the process- PLEDs are the expression of neural net- tions that do not influence shorter interictal- es driving PLEDs. Anesthetizing the work dysfunction producing cortical hyper- like events.44-46 In rodent hippocampal patient, increasing the depth of anesthesia, synchrony at a rate of about 1/s. It is not slices, AEDs resulted in truncation of long- or combining anesthetics in order to sup- clear what neurodynamic perturbations give lasting seizure-like discharges elicited by press PLEDs may therefore be more harm- rise to PLEDs, much less whether these per- long-duration high-frequency stimulation, ful than beneficial to the patient. turbations are interictal, ictal, or nonepilep- but did not affect short-lived IED-like activ- As a rule, DIBS is bihemispheric, tic in nature. It is for this reason that a non- ity induced by stimulation every 5 to10 sec- bisymmetric, and bisynchronous in adults. committal term, such as LPDs, is preferred onds.47 Some well-controlled studies Asymmetric and/or asynchronous DIBS has over PLEDs.27,28 In 1950, Cobb et al. attrib- showed that AED levels that control been reported in patients with disorders uted periodic discharges to a disconnection seizures do not suppress focal IEDs.48,49 involving the corpus callosum.54,55 of the cerebral cortex from subcortical Recently, Guida et al. published a review of However, true unihemispheric burst sup- structures.36 After studying autopsy speci- past studies that sought to determine the pression (UBS) is rare. Recently, we report- mens, Chatrian et al. found no anatomic effects of AEDs (alone or in combination) ed two cases in which administration of isolation of cortical areas involved in gener- on focal IEDs and concluded that the data is propofol to terminate ongoing status epilep- ating PLEDs and the putative lesions were scarce or conflicting for classical AEDs and ticus resulted in the appearance of UBS.56 frequently far from the cortical generator.1 absent or limited for newer AEDs.50 In any In both patients, UBS occurred ipsilateral to

[page 4] [Neurology International 2017; 9:6933] Case Report a structural brain lesion and disappeared smaller set of intermediate frequencies. 2000;111:2125-9. when the propofol infusion rate was This process, which Kalamangalam et al. 7. Westmoreland BF, Frere RC, Klass DW. increased indicating an epileptic mecha- refer to as spectral condensation, can serve Periodic epileptiform discharges in the nism.56 As an EEG finding, UBS challenges as a framework for understanding all nor- midline. J Clin Neurophysiol 1997;14: the prevailing view that burst suppression is mal and abnormal, rhythmic and periodic, 495-8. global with widespread synchronous and synchronous cortical activity.62,63 8. Bertolucci PH, Silva AB. Alternating homogenous cortical activation during burst periodic lateralized epileptiform dis- episodes and inactivation during periods of charges (cerebral bigeminy). Clin suppression.57 The theory that DIBS is root- Electroencephalogr 1992;23:177-9. ed in local neurodynamics was put forth as Conclusions 9. García-Morales I, García MT, Galán- early as 1952.58 That DIBS is an expression Dávila L, et al. Periodic lateralized PLEDs can survive anesthesia and per- of local cortical dynamics is supported by a epileptiform discharges: etiology, clini- sist during DIBS as PLEDs fragments or recent intracranial EEG study of patients cal aspects, seizures, and evolution in remnants that give DIBS an asymmetric under propofol anesthesia which showed 130 patients. J Clin Neurophysiol 2002; appearance. This may be subtle and can be asynchronous expression of DIBS in differ- 19:172-7. easily overlooked if the EEG during DIBS ent cortical areas and restriction of DIBS in 10. Fitzpatrick W, Lowry N. PLEDs: clini- is not carefully inspected and compared some cortical areas with other areas exhibit- cal correlates. Can J Neurol Sci with the preanesthesia EEG. The PLEDs ing continuous activity.59 2007;34:443-50. fragments are mixed with other burst com- Abnormal neuronal network dynamics 11. Andraus ME, Andraus CF, Alves-Leon ponents but continue to exhibit some of the underlies cortical hypersynchrony in SV. Periodic EEG patterns: importance original characteristics of PLEDs, such as patients with epilepsy.60,61 The idea of an of their recognition and clinical signifi- spatial distribution and morphology. This interictal-ictal continuum was contrived cance. Arq Neuropsiquiatr 2012;70: finding suggests that PLEDs, DIBS, and because some forms of cortical hypersyn- 145-51. other periodic EEG patterns share some chrony could not be classified as interictal 12. Baykan B, Kinay D, Gökyigit A, Gürses basic neurodynamic mechanisms. or ictal.12,15 Some studies showed the risk C. Periodic lateralized epileptiform dis- Physicians, who are aware of the difficulty only of seizures to be higher in PLEDs-plus than charges: association with seizures. of suppressing PLEDs during the acute in PLEDs-proper.14,15 It is possible (there Seizure 2000;9:402-26. phase of a brain disorder, can avoid expos- are no studies) that UBS carries a higher 13. Pohlmann-Eden B, Hoch DB, Cochius ing patients to the risk of anesthesia. The risk of seizures than PLEDs-plus and that JI, Chiappa KH. Periodic lateralized pathophysiological and therapeutic signifi- the unihemispheric periodic patterns – use epileptiform discharges: a critical cance of burst-embedded PLEDs fragments PLEDs-proper, PLEDs-plus, and UBS – review. J Clin Neurophysiol 1996;13: and their tenacity to anesthesia deserve fur- represent an interictal-ictal continuum. We 519-30. ther investigation. also believe that DIBS is rooted in local cor- 14. Garzon E, Fernandes RM, Sakamoto tical dynamics and that different periodic AC. Serial EEG during human status EEG patterns involve the same fundamental epilepticus: evidence for PLED as an oscillatory mechanisms. Kalamangalam et References ictal pattern. Neurology 2001 al. reviewed the CT/MRI of 106 patients 9;57:1175-83. with PLEDs and found PLEDs to be longer 1. Chatrian GE, Shaw CM, Leffman H. 15. Reiher J, Rivest J, Grand'Maison F, in duration and more variable in morpholo- The significance of periodic lateralized Leduc CP. Periodic lateralized epilepti- gy when the cause is a cortical lesion than epileptiform discharges in EEG: an form discharges with transitional rhyth- when it is a subcortical lesion.62 The authors electrographic, clinical and pathological mic discharges: association with offered a unified view of periodic EEG pat- commercialstudy. Electroencephalogr Clin seizures. Electroencephalogr Clin terns – they proposed that PLEDs from sub- Neurophysiol 1964;17:177-93. Neurophysiol 1991;78:12-7. cortical lesions and generalized periodic 2. Brenner RP, Schaul N. Periodic EEG 16. Chong DJ, Hirsch LJ. Which EEG pat- EEG patterns from severe metabolic dis- patterns: classification, clinical correla- terns warrant treatment in the critically eases share common pathogeneticNon mecha- tion, and pathophysiology. J Clin ill? Reviewing the evidence for treat- nisms. In another study, Kalamangalam et Neurophysiol 1990;7:249-67. ment of periodic epileptiform dis- al. compared the frequency components of 3. de la Paz D, Brenner RP. Bilateral inde- charges and related patterns. J Clin PLEDs and the EEG background and con- pendent periodic lateralized epilepti- Neurophysiol 2005;22:79-91. cluded that pathological processes can lead form discharges. Clinical significance. 17. Sen-Gupta I, Schuele SU, Macken MP, to the emergence of PLEDs from the back- Arch Neurol 1981;38:713-5. et al. "Ictal" lateralized periodic dis- ground by means spectral condensation.62 4.Silbert PL, Radhakrishnan K, charges. Epilepsy Behav 2014;36:165- Normal or pathological states that influence Sharbrough FW, Klass DW. Ipsilateral 70. the spatiotemporal organization of local independent periodic lateralized epilep- 18. Handforth A, Cheng JT, Mandelkern field cortical potentials and cause functional tiform discharges. Electroencephalogr MA, et al. Markedly increased cortical domains to expand or contract can Clin Neurophysiol 1996;98:223-6. mesiotemporal lobe metabolism in a alter the frequencies and rhythms of the 5. Hughes JR, Taber J, Uppal H. TRI- case with PLEDs: further evidence that EEG. Pathological processes that enhance PLEDs: a case report. Clin PLEDs are a manifestation of partial excitatory or reduce inhibitory neurotrans- Electroencephalogr 1998;29:106-8. status epilepticus. Epilepsia mission in the cortex may lead to coupling 6.Lawn ND, Westmoreland BF, 1994;35:876-81. of cortical domains, both in spatial terms Sharbrough FW. Multifocal periodic 19. Assal F, Papazyan JP, Slosman DO, et and in terms of their intrinsic frequencies. lateralized epileptiform discharges al. SPECT in periodic lateralized When rhythms merge, the multi-frequency (PLEDs): EEG features and clinical epileptiform discharges (PLEDs): a mix gives way to global synchrony at some correlations. Clin Neurophysiol form of partial status epilepticus?

[Neurology International 2017; 9:6933] [page 5] Case Report

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