•Complications from standard ATL are uncommon and the use of post-operative corticosteroids may reduce complications.•Following standard ATL, FMSE was present after treatment with corticosteroids that resolved after blood sugar control.•After epilepsy surgery, corticosteroids should be used cautiously in people with comorbid diabetes mellitus

Air, Ellen L

Alshammaa, Abdullah

Kahn, Muhammad S

Madani, Sarah

Zahoor, Salman

Zillgitt, Andrew

English

Henry Ford Health System Scholarly Commons

Henry Ford Health System Henry Ford Health System Scholarly Commons Neurosurgery Articles Neurosurgery 1-1-2018 Post-operative nonketotic hyperglycemic induced focal motor status epilepticus related to treatment with corticosteroids following standard anterior temporal lobectomy. Andrew Zillgitt Abdullah Alshammaa Muhammad S. Kahn Sarah Madani Salman Zahoor See next page for additional authors Follow this and additional works at: https://scholarlycommons.henryford.com/neurosurgery_articles Recommended Citation Zillgitt A, Alshammaa A, Kahn MS, Madani S, Zahoor S, and Air EL. Post-operative nonketotic hyperglycemic induced focal motor status epilepticus related to treatment with corticosteroids following standard anterior temporal lobectomy. Epilepsy Behav Case Rep 2018; 10:124-128. This Article is brought to you for free and open access by the Neurosurgery at Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Neurosurgery Articles by an authorized administrator of Henry Ford Health System Scholarly Commons. Authors Andrew Zillgitt, Abdullah Alshammaa, Muhammad S. Kahn, Sarah Madani, Salman Zahoor, and Ellen L. Air This article is available at Henry Ford Health System Scholarly Commons: https://scholarlycommons.henryford.com/neurosurgery_articles/135 Case ReportPost-operative nonketotic hyperglycemic induced focal motor statusepilepticus related to treatment with corticosteroids following standardanterior temporal lobectomyAndrew Zillgitt a,⁎, Abdullah Alshammaa b, Muhammad Salim Kahn b, Sarah Madani b,Salman Zahoor b, Ellen L. Air ca Department of Neurology, Beaumont Health, Royal Oak, MI, USAb Department of Neurology, Henry Ford Health System, Detroit, MI, USAc Department of Neurosurgery, Henry Ford Health System, Detroit, MI, USAa r t i c l e i n f oArticle history:Received 11 June 2018Received in revised form 28 August 2018Accepted 4 September 2018Available online 2 October 20181. IntroductionIn cases of drug-resistant unilateral mesial temporal lobe epilepsy(MTLE) due to hippocampal sclerosis, standard anterior temporal lobec-tomy (ATL) may result in seizure freedom in over 65% of cases [1–5].Complications from standard ATL are relatively uncommon. However, inless than 6% of cases complications could include stroke, subdural hema-toma, new neurologic deficits, postoperative infections, and/or cognitiveand behavioral changes [5]. The use of post-operative corticosteroidsmay mitigate post-operative symptoms, e.g., headache, and limit othercomplications [6–8]. In individuals with diabetes, caution must beemployed when using corticosteroids to reduce complications related toelevated blood glucose. One common presentation of nonketotic hyper-glycemic states is focal motor status epilepticus or epilepsia partialis con-tinua (EPC) [9–12]. However, post-operative corticosteroid-induced focalmotor status epilepticus following standard ATL has been less commonlydescribed. This case report describes a patient with postoperativenonketotic hyperglycemic induced focal motor status epilepticus relatedto treatment with corticosteroids following standard ATL.2. Case ReportA 31-year-old right-handed woman presented to the Henry FordHealth System Comprehensive Epilepsy Program with a history ofdrug-resistant focal epilepsy. Her index seizure was a focal to bilateraltonic–clonic seizure at the age of 15 years old that occurred inthe setting of eclampsia. She was placed on a trial of levetiracetamand remained seizure-free until the age of 23 years old when sheexperienced a focal impaired awareness seizure. Following thisseizure, her seizures remained resistant to anti-seizure drug trials oflevetiracetam, lamotrigine, clobazam, zonisamide, lacosamide, carba-mazepine XR, and perampanel.Her habitual seizures began with a feeling of nausea or a risingsensation in her abdomen. After this she would lose awareness duringwhich time manual and oral automatisms would occur. Additionally,ictal spitting could be present. On rare occasions her focal seizurescould evolve to a bilateral tonic–clonic seizure with versive headmove-ments to the right and left upper extremity tonic posturing.Her noninvasive diagnostic studies, including inpatient video-EEGmonitoring, brain MRI, FDG-PET, and neuropsychology testing, wereconcordant and implicated an epileptogenic zone within the righttemporal lobe (Figs. 1–3). In light of these findings, a right standardATL was completed (Fig. 4). Her immediate post-operative course wasuncomplicated, and she was discharged home on the second post-operative day. At discharge, her anti-seizure medication regimenconsisted of lacosamide 200mg in the morning and 300mg at bedtimeand perampanel 6 mg at bedtime. She was also placed on dexametha-sone 4 mg every 6 h with a tapering schedule of 4 mg every 3 days for12 days followed by 2 mg daily for 3 days before discontinuing thistreatment. Her anti-seizuremedicationswere not tapered after surgery,and she initially tolerated treatment with dexamethasone well withoutadverse reactions.Then approximately oneweek following her discharge, she began toexperience seizures that were different than her habitual seizures.These new seizures consisted of frequent, brief focal motor seizurescharacterized by repetitive left hemi-facial contractionswithout impair-ment of awareness. She was urgently admitted to Henry Ford Hospitalfor further evaluation and management. A repeat brain MRI demon-strated postsurgical changes in the right anterior temporal lobewith ad-jacent increased T2/FLAIR signal along the superior and posteriorresection cavity (Fig. 4A-C). Continuous video-EEGmonitoring revealedfocal motor status epilepticus with seizures arising from the rightEpilepsy & Behavior Case Reports 10 (2018) 124–128⁎ Corresponding author at: Department of Neurology, Neuroscience Center, 3555West13 Mild Road, Suite N120, Royal Oak, MI 48073, USA.E-mail address: Andrew.Zillgitt@beaumont.org (A. Zillgitt).Contents lists available at ScienceDirectEpilepsy & Behavior Case Reportsj ourna l homepage: www.e lsev ie r .com/ locate /ebcrhttps://doi.org/10.1016/j.ebcr.2018.09.0012213-3232/© 2018 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).fronto-central region (Figs. 5 and 6). She continued to experience ap-proximately 17 seizures every 6 hours and a loading dose levetiracetamwith escalating doses of lacosamide and perampanel were unsuccessfulin controlling her seizures.Review of her laboratory findings revealed markedly elevated bloodglucose of 445mg/dL (range 50–150). Prior to surgery her blood glucosewas 136 mg/dL and at discharge from HFH her blood glucose was113mg/dL (Table 1). During this admission, she relayed a prior diagno-sis of type II diabetes mellitus that resolved following 200-poundweight loss approximately 10 years prior. Upon further review, shealso required treatment for gestational diabetes with metformin twoyears prior to ATL.Fig. 1. Interictal EEG; Right temporal sharp-and-wave discharge during stage 2 sleep. AP bipolar montage, TC 0.3, HFF 70 Hz, Sen 7 uV.Fig. 2. Ictal EEG; Right temporal lobe seizure, 30 seconds after clinical onset. AP bipolar montage, TC, 0.1, HFF 70 Hz, Sen uV.125A. Zillgitt et al. / Epilepsy & Behavior Case Reports 10 (2018) 124–128With aggressive control of her blood glucose, including a trial ofmetformin and discontinuation of dexamethasone, her new seizures im-proved and subsequently resolved. She had no recurrent focal motor sei-zures after this and she has been free of her habitual seizures for over3 years.3. DiscussionIn this case, a woman with drug resistant focal epilepsy had concor-dant noninvasive diagnostic testing that implicated an epileptogeniczone within the right temporal lobe. Following a right standard ATLshe experienced a new seizure-type that occurred in the setting oftreatment with dexamethasone. She subsequently disclosed a priordiagnosis of type II diabetes mellitus that had previously beenmanagedwith weight loss and exercise. After aggressive control of her blood glu-cose, these new seizures decreased in frequency and resolved. She hasremained free of her habitual focal impaired awareness seizures andher postoperative focal motor seizures for over 3 years.Focal motor status epilepticus or EPC are common and oftenthe presenting sign in nonketotic hyperglycemic states [12,13]. Interest-ingly, in this case the focal motor seizures arose from the same hemi-sphere as the resection site. Although this may raise concerns for anindependent seizure onset zone or false localization of the hypothesizedpresurgical epileptogenic zone, one case series of 22 patients with EPCin the setting of hyperglycemia identified a structural lesion in themajority of subjects [13]. In this case, it would be less likely theseFig. 3. A-B – Preoperative brain MRI (coronal FLAIR sequence); there is atrophy, loss of internal architecture, and increased FLAIR signal within the right mesial temporal structures andhippocampus.Fig. 4.A-C – Post-operative brainMRI (A – coronalmagnetization-prepared rapid gradient-echo (MP-RAGE), B – axial MP-RAGE, C – sagittalMP-RAGE); there are post-surgical changes inthe right temporal lobe without obvious structural abnormalities within the adjacent right frontal and temporal lobes.126 A. Zillgitt et al. / Epilepsy & Behavior Case Reports 10 (2018) 124–128seizureswere due to perioperative focal seizure aggravation in the fron-tal neocortex with asymptomatic glucose elevation. Rather, in the set-ting of a structural abnormality, hyperglycemia from treatment withdexamethasone could have contributed to the onset of postoperativefocal motor status epilepticus.Early seizure recurrence after epilepsy surgery may suggest failureto adequately resect or disconnect the epileptogenic zone [14]. How-ever, the seizures in this caseweremarkedly different thanher preoper-ative seizure semiology. Additionally, early studies reviewing criteria forlocalizing an epileptogenic focus reported focal functional deficitsFig. 5. Post-operative ictal EEG; Right fronto-central seizures, 15 seconds after EEG and clinical onset. AP bipolar montage, TC 0.1, HFF 70 Hz, Sen 7 uV.Fig. 6. Post-operative ictal EEG density spectral array (DSA) trend; there was a total of 17 focal motor seizures over this 6-hour time period; TC 0.1, HFF 70 Hz, Sen 7 uV.127A. Zillgitt et al. / Epilepsy & Behavior Case Reports 10 (2018) 124–128provided beneficial nonconflicting confirmatory information [15].In this regard, FDG-PET could be useful in the epilepsy presurgicalevaluation. A review of epilepsy networks by Spencer in 2002 notedhypometabolism on FDG-PET is a consistent finding in MTLE and its ab-sence should raise doubt to accurate localization of an epileptic networkwithin the medial temporal structures [16]. Therefore, if there was nohypometabolism within the right temporal lobe on FDG-PET, consider-ation should be given to an epileptic network outside of this region. Thiswas not the case in this patient where FDG-PET demonstratedhypometabolism within the right temporal lobe.A recent prospective study evaluated the utility of inpatient video-EEG monitoring in people with suspected MTLE associated with unilat-eral MTS [17]. In this study, there was no difference in seizure outcomeafter surgery between the groups who had video-EEG monitoring andthosewhodid not. The authors suggested it could be safe to recommendepilepsy surgery without inpatient video-EEG monitoring in peoplewith MTLE with unilateral MRI signs of MTS, clinical semiology consis-tent with MTLE, no suspicion of nonepileptic events, and adequate out-patient EEGswith lateralized interictal epileptiform activity toMTS [17].The patient in this case demonstratedmany of these characteristics, andthis would strengthen the hypothesis of right MTLE as opposed to anepileptic network within the right frontal central region.Despite the concordant noninvasive diagnostic testing implicatingan epileptogenic zonewithin the rightmesial temporal lobe, “secondaryepileptogenesis” could produce an independent, de novo, epileptogenicfocus. However, this phenomenon has not been described in thehyperacute post-operative period [14]. In fact, secondary epileptogenesisis believed to be a phenomenon that occurs often over 12 months afterepilepsy surgery [14].Therefore, in light of a preoperative seizure semiology consistentwith mesial temporal lobe seizures, unilateral right MTS on structuralbrain MRI, the presence of right temporal lobe hypometabolism onFDG-PET, and markedly different seizure semiology between pre- andpost-operative seizures, a diagnosis of right MTLE is favored over anoverlooked epileptic network within the right frontal central sulcus.Furthermore, the improvement in her seizure frequency after blood glu-cose control would suggest the new seizures in this caseweremost likelyrelated to elevated blood glucose from treatment with dexamethasone.Overall, complications from epilepsy surgery, and particularly ATL,are relatively uncommon. Previous studies have estimated complicationrates around 6–10% in all surgical cases, and more recent studies havesuggested the complication rates may be significantly lower at high-volume, compared to low-volume, epilepsy surgical centers [3–5,7,8].However, a recent review of CMS Part B data and the NationalSurgical Quality Improvement Program (NIQSIP) database, reportedcomplications in nearly 18% of surgical cases [7]. Complications weremore common in older individuals, male gender, those with higherAmerican Society of Anesthesiologists (ASA) classification, and inthose people with a pre-existing bleeding disorder [7]. The mostcommon complication was a return to the operating room (primarilyfor hemorrhage), but complications ranged from death and cardiac arrestto septic shock and deep vein thrombosis [7].Treatment with corticosteroids following ATL dates back to the1960's [6]. The use of corticosteroids may reduce cerebral edema andother perioperative complications. However, the use of corticosteroidsin people with diabetes mellitus may result in elevated blood glucoseand serum osmolality. In cases of nonketotic hyperglycemic states,seizures, and specifically focalmotor seizures,may be common and a pre-senting feature [9–12]. The mechanism behind seizures due to elevatedblood glucose and serum osmolality is poorly understood, but some stud-ies have suggested glucose is a “pro-convulsant,” [12]. Interestingly, 20people had comorbid diabetesmellitus, and an additional 35were receiv-ing chronic steroids [7]. Six of the 20peoplewith comorbiddiabetes expe-rienced complications, while ten out of thirty-five people with chronicsteroid use also had a complication [7]. There was no report of focalmotor status epilepticus or EPC in this database review [7].ConclusionsThis case demonstrates a previously unreported potential complica-tion following an ATL. Overall, complications after ATL are relativelyrare, and corticosteroidsmaymitigate some postoperative complications.In people undergoing epilepsy surgery, corticosteroids should be usedcautiously in people with comorbid diabetes mellitus to avoid nonketoichyperglycemic states. Aggressive blood glucose control in the post-operative period may reduce surgical complications and the potentialfor post-operative corticosteroid-induced focal motor status epilepticus.References[1] Tatum 4th WO. Mesial temporal lobe epilepsy. J Clin Neurophysiol 2012;29(5):356–65.[2] Engel Jr J, McDermott MP, Wiebe S, Langfitt JT, Stern JM, Dewar S, et al. Early surgicaltherapy for drug-resistant temporal lobe epilepsy: A randomized trial. JAMA 2012;307(9):922–30.[3] Wiebe S, Blume WT, Girvin JP, Eliasziw M. Effectives and Efficiency of Surgery forTemporal Lobe Epilepsy Study Group. A randomized, controlled trial of surgery fortemporal-lobe epilepsy. N Engl J Med 2001;345(5):311–8.[4] Wiebe S, Jette N. Pharmacoresistance and the role of surgery in difficult to treat ep-ilepsy. Nat Rev Neurol 2012;8(12):669–77.[5] Engel Jr J, Wiebe S, French J, Sperling M, Williamson P, Spencer D, et al. Practice pa-rameter: Temporal lobe and localized neocortical resections for epilepsy: Report ofthe Quality Standards Subcommittee of the American Academy of Neurology, in as-sociation with the American Epilepsy Society and the American Association of Neu-rological Surgeons. Neurology 2003;60(4):538–47.[6] Rasmussen T, Gulati DR. Cortisone in the treatment of postoperative cerebral edema.J Neurosurg 1962;19:535–44.[7] Rolston JD, Englot DJ, Knowlton RC, Chang EF. Rate and complications of adult epi-lepsy surgery in North America: Analysis of multiple databases. Epilepsy Res 2016;124:55–62.[8] Englot DJ, Ouyang D, Wang DD, Rolston JD, Garcia PA, Change EF. Relationship be-tween hospital surgical volume, lobectomy rates, and adverse perioperative eventsat US epilepsy centers. J Neurosurg 2013;118(1):169–74.[9] Singh BM, Strobos RJ. Epilepsia partialis continua associatedwith nonketotic hypergly-cemia: Clinical and bio-chemical profile of 21 patients. Ann Neurol 1980;8:155–60.[10] Hennis A, Corbin D, Fraser H. Focal seizures and non-ketotic hyperglycemia. J NeurolNeurosurg Psychiatry 1992;55:195–7.[11] Hwang KJ, Yoon S, Park KC. Non-ketotic hyperglycemia presenting as epilepsiapartialis continua. Epileptic Disord 2016;18(2):201–3.[12] HungWl, Hsieh PF, Lee YC, ChangeMH. Occipital lobe seizures related to marked el-evation of hemoglobin A1C: Report of two cases. Seizure 2010;19(6):359–62.[13] Paiboonpol S. Epilepsia partialis continua as a manifestation of hyperglycemia. J MedAssoc Thail 2005;88(6):759–62.[14] Najm I, Jehi L, Palmini A, Gonzalez-Martinez J, Paglioi E, BingamanW. Temporal pat-terns and mechanisms of epilepsy surgery failure. Epilepsia 2013;54(5):772–82.[15] Engel Jr J, Rausch R, Lieb JP, Kuhl DE, Crandall PH. Correlation of criteria used for lo-calizing epileptic foci in patients considered for surgical therapy of epilepsy. AnnNeurol 1981;9(3):215–24.[16] Spencer SS. Neural networks in human epilepsy: Evidence of and implications fortreatment. Epilepsia 2002;43(3):219–27.[17] AlvimMKM, Morita ME, Yasuda CL, Damasceno BP, Lopes TM, Coan AC, et al. Is inpa-tient ictal video-electroencephalographic monitoring mandatory in mesial temporallobe epilepsy with unilateral hippocampal sclerosis? A prospective study. Epilepsia2018;59:410–9.Table 1Serum glucose pre-and-post right standard ATL.Date Serum glucose3 months prior to surgery 136 mg/dL (range 50–140)Day of surgery 176 mg/dL (range 50–140)2 weeks post right standard ATL 445 mg/dL (range 50–140)3 weeks post right standard ATL after treatment 113 mg/dL (range 50–140)6 months post right standard ATL(treatment with metformin)106 mg/dL (range 60–99)30 months post right standard ATL(treatment with metformin)121 mg/dL (range 60–99)128 A. 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Post-operative nonketotic hyperglycemic induced focal motor status epilepticus related to treatment with corticosteroids following standard anterior temporal lobectomy

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Post-operative nonketotic hyperglycemic induced focal motor status epilepticus related to treatment with corticosteroids following standard anterior temporal lobectomy

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