| Article Access Statistics|
| Viewed||1416 |
| Printed||16 |
| Emailed||0 |
| PDF Downloaded||32 |
| Comments ||[Add] |
Click on image for details.
|Year : 2021 | Volume
| Issue : 3 | Page : 733-736
Non-Convulsive Status Epileptics Presenting with Periodic Lateralized Epileptiform Discharges and Coma after Cerebral Hemorrhage: A Case Report
Zhuo Wang1, Chaojia Chu1, Chaoyang Jing2, Xiangyu Zheng1, Weihong Lin1
1 Department of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun, China
2 Department of Neurology, The Huaihe Hospital of Henan University, Kaifeng, Henan, China
|Date of Submission||30-Jun-2017|
|Date of Decision||20-Aug-2019|
|Date of Acceptance||16-Mar-2021|
|Date of Web Publication||31-May-2021|
Dr. Weihong Lin
Department of Neurology and Neuroscience Center, The First Hospital of Jilin University, Changchun - 130 021, Jilin
Source of Support: None, Conflict of Interest: None
Background: Non-convulsive status epileptics (NCSE) is a common neurological emergency necessitating rapid assessment and management, but is often underdiagnosed as it lacks specific electroencephalographic features. The diagnostic value of periodic lateralized epileptiform discharges (PLEDs) in NCSE is still unclear. Herein, we reported a case with NCSE manifesting as PLEDs and coma.
Case Report: A 62-year-old man presented with epileptic seizures. Based on clinical and radiological profiles, he was diagnosed with frontal hemorrhage, coma, and NCSE. An electroencephalogram (EEG) revealed PLEDs. A combined antiepileptic regimen was initiated and, over a follow-up period of 2 months, a favorable outcome was achieved.
Conclusion: EEG may help identify potential NCSE in comatose patients, and PLEDs can be an atypical manifestation of NCSE, which can be effectively treated with antiepileptic drugs. The emphasis in NCSE is on early identification and individualized therapeutic regimens.
Keywords: Case report, cerebral hemorrhage, coma, non-convulsive status epileptics, periodic lateralized epileptiform dischargesKey Message: Non-convulsive status epileptics manifesting as periodic lateralized epileptiform discharges and coma can be identified by EEG and effectively treated with antiepileptic drugs.
|How to cite this article:|
Wang Z, Chu C, Jing C, Zheng X, Lin W. Non-Convulsive Status Epileptics Presenting with Periodic Lateralized Epileptiform Discharges and Coma after Cerebral Hemorrhage: A Case Report. Neurol India 2021;69:733-6
|How to cite this URL:|
Wang Z, Chu C, Jing C, Zheng X, Lin W. Non-Convulsive Status Epileptics Presenting with Periodic Lateralized Epileptiform Discharges and Coma after Cerebral Hemorrhage: A Case Report. Neurol India [serial online] 2021 [cited 2021 Jul 27];69:733-6. Available from: https://www.neurologyindia.com/text.asp?2021/69/3/733/317237
Status epilepticus is an epileptic seizure lasting for more than 5 min, or more than 1 seizure occurring within a 5-min period without interictal return to normalcy. Status epilepticus can be divided into two forms, convulsive or non-convulsive status epilepticus (NCSE). NCSE refers to a prolonged consciousness change without large-scale bending and extension of the limbs. As reported, NCSE constitutes up to a quarter of all status epilepticus cases, with an incidence of approximately 8% in all comatose patients. The diagnosis of NCSE, which mainly depends on clinical status and electroencephalogram (EEG) findings, is challenging, especially in comatose patients. NCSE is often underdiagnosed as it lacks characteristic electroencephalographic findings. The diagnostic value of nonspecific ictal or interictal EEG features in NCSE, particularly periodic lateralized epileptiform discharges (PLEDs), remain unclear. Herein, we reported a case in coma with NCSE manifesting as PLEDs.
| » Case Report|| |
A 62-year-old man was admitted to our department with epileptic seizures. Five hours before admission, the patient was found lying on the bathroom floor with trembling limbs, eyes rolled up, drooling from the mouth, with sphincter incontinence. The patient experienced 5--6 episodes of seizures, each lasting for 10 s and at intervals of 2--3 min. The patient had a 20-year history of hypertension, arthrolithiasis, and alcohol consumption. There was no history of epilepsy, intracranial infection, febrile convulsion, or trauma. Family history was unremarkable. On admission, the blood pressure was normal, and heart rate was 130 beats/min. The patient was in moderate coma (Glasgow Coma Score = 7), and tracheal intubation was done. Pupils were round, normal in size, and pupillary light reflexes were positive bilaterally. Muscular tone in the extremities was normal and bilateral pathological signs were absent; other neurological examinations could not be undertaken because of the comatose condition of the patient. Brain computed tomography (CT) showed a hemorrhage in the right frontal lobe [Figure 1]a. Brain magnetic resonance venography (MRV) excluded sinus thrombosis. Diazepam and phenobarbital were administered via intravenous (IV) and intramuscular (IM) injections, respectively, and a sodium valproate IV infusion pump was set up (15 mg/kg by IV injection in the first 3--5 min, and 1 mg/kg/h in the following continuous IV infusion). The patient developed twitching in the angulusoris and periocular areas, which lasted for 30 s and resolved spontaneously. Four days later, the patient was seizure free but slipped into a persistent coma. Video EEG monitoring revealed medium- to high-amplitude spike–slow wave and sharp–slow wave complexes, which originated predominantly from the right temporal lobe at intervals of 1 s. These EEG findings were consistent with PLEDs [Figure 2]. Brain magnetic resonance imaging (MRI) showed extensive edema in the right-side cerebral cortex [Figure 3]. Based on these findings, the patient was diagnosed with frontal hemorrhage, coma, and NCSE. EEG monitoring after IV diazepam 10 mg demonstrated that PLEDs were significantly inhibited [Figure 4]. However, as the PLEDs recurred repeatedly, oral levetiracetam and topiramate were added. CT scanning on days 3 and 6 during hospitalization showed the hematoma had gradually been absorbed [Figure 1]b and [Figure 1]c, whereas EEG revealed persistent PLEDs. By Day 11, electroencephalographic abnormalities had disappeared [Figure 5]; the patient's level of consciousness improved and the tracheal cannula was removed. One month later, brain CT [Figure 1]d and MRI [Figure 6] showed the hematoma had resolved with remnant perilesional edema. At the 2-months follow-up, the patient was well oriented, and rehabilitative treatment was continued.
|Figure 1: Brain CT of the patient (a) Axial CT showed an irregular hyperdensity in the right frontal lobe surrounded by perilesional hypodensity. (b and c) Repeated CT scanning showed the hematoma was gradually absorbed. (d) Follow-up CT revealed the hematoma was completely resolved with remnant edema|
Click here to view
|Figure 2: EEG of the patient on admission. EEG monitoring revealed PLEDs originated predominantly from the right frontotemporal lobe|
Click here to view
|Figure 3: Brain MRI of the patient on admission. Diffusion-weighted imaging showed multifocal hyperintensities in the right cortex, hippocampus, and basal ganglia (arrows)|
Click here to view
|Figure 4: EEG of the patient after administration of diazepam. EEG revealed PLEDs were significantly inhibited|
Click here to view
|Figure 5: EEG of the patient on Day 11 after admission. EEG demonstrated no remarkable abnormalities|
Click here to view
|Figure 6: Brain MRI of the patient 1 month after admission. Diffusion-weighted imaging showed persistent hyperintensity in the right frontal lobe, and that the other abnormal signals had disappeared|
Click here to view
| » Discussion|| |
Status epilepticus, the most serious form of seizure, is a medical emergency, as it may lead to permanent brain damage. NCSE is extremely severe, carrying major morbidity and mortality. Clinical manifestations of NCSE can vary from a mild confusion to a coma; in severe cases, individuals may resemble many other coma patients who are unresponsive due to an encephalopathy or other disorders of consciousness. This distinction should be emphasized because status epilepticus may respond to antiepileptic medications, and EEG may help the differential diagnosis. In 2004, the Epilepsy Foundation of America Working Group defined NCSE as a range of conditions in which electrographic seizure activity is prolonged and results in non-convulsive clinical symptoms. The main points of diagnosis proposed in previous studies included: (1) deterioration of consciousness status, or presence of a coma; (2) absence of motor deficiency, or subtle motor findings such as perioral or eyelid twitching; and (3) EEG showing continuous or repetitive epileptiform activity for longer than 30 min. In the current case, the patient had no previous history of epilepsy; based on clinical and radiological profiles, a diagnosis of cerebral hemorrhage and secondary brain dysfunction was confirmed. Notably, the onset symptom was convulsive status epilepticus, and the patient gradually slipped into a persistent coma; meanwhile, EEG showed PLEDs, which improved on subsequent diazepam treatment. These features were consistent with NCSE.
PLEDs were first described by Chatrian et al. in 1964, denoting large (50--300 μV or higher), sharp, and repetitive (usually close to 1 Hz) discharges on scalp EEG. PLEDs are usually seen in patients with epileptic seizures, acute structural brain lesions, or metabolic disorders, and they are often distributed over a unilateral hemisphere. Neufeld et al. proposed that PLEDs in patients with acute stroke might be triggered by metabolic disturbances such as hyperglycemia and fever. In our case, the hematoma in the frontal lobe was limited, reflecting slight structural changes, suggesting that PLEDs may be induced by NCSE-related metabolic disturbances.
A definitive association between PLEDs and NCSE as well as the pathophysiological mechanisms of PLEDs remains unclear, especially with regard to the cause of periodicity. Lawn et al. speculated that acute structural lesions and metabolic disorders might lead to partial deafferentation of the cerebral cortex and subsequent alteration of cortical function, and these dysfunctions could cause enhanced neuronal excitability and impaired inhibitory mechanisms resulting in repetitive epileptiform discharges. Our patient had concomitant cortical edema, which resolved together with the improvement in consciousness, indicating that altered consciousness may have been related to structural edema. This phenomenon can also be attributed to cerebral deafferentation and enhancement of neuronal excitability.
PLEDs in coma patients are frequent, whereas the diagnostic values of PLEDs in distinguishing between NCSE and coma are yet to be elucidated. Some scholars have proposed that PLEDs may be an EEG manifestation of NCSE, whereas others hold that PLEDs only reflect severe encephalopathy rather than a specific feature of epileptic seizure. In the current case, EEG monitoring showed dynamic changes that significantly improved after IV diazepam administration. We infer, therefore, that diagnostic treatment with antiepileptic drugs is important for the identification of NCSE.
The management of NCSE accompanying with coma is controversial. Litt et al.proposed that IV injection of antiepileptic drugs such as benzodiazepine and midazolam should be used for NCSE patients, especially for patients with severe loss of consciousness, as potential NCSE can progress toward intractable status epilepticus. However, some researchers found IV diazepam administration to be associated with risks of hypotension, hyperventilation, and arrhythmia. Herein, we recommend the usage of IV diazepam under video EEG monitoring to prevent overdose, extended hospital stay, and ventilator-related complications. In our case, a favorable prognosis was achieved with medical management.
| » Conclusion|| |
EEG may help identify potential NCSE in coma patients, and PLEDs can be a nonspecific electrophysiological manifestation of NCSE. Antiepileptic drugs are effective for treating this condition. Early diagnosis and individual treatment, especially in the elderly, are emphasized in the effective management of NCSE.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| » References|| |
Towne AR, Waterhouse EJ, Boggs JG, Garnett LK, Brown AJ, Smith JR, et al
. Prevalence of nonconvulsive status epilepticus in comatose patients. Neurology 2000;55:1421-3.
Alroughani R, Javidan M, Qasem A, Alotaibi N. Non-convulsive status epilepticus; The rate of occurrence in a general hospital. Seizure 2009;18:38-42.
Akman CI. Nonconvulsive status epilepticus and continuous spike and slow wave of sleep in children. Semin Pediatr Neurol 2010;17:155-62.
Neufeld MY, Vishnevskaya S, Treves TA, Reider I, Karepov V, Bornstein NM, et al
. Periodic lateralized epileptiform discharges (PLEDs) following stroke are associated with metabolic abnormalities. Electroencephalogr Clin Neurophysiol 1997;102:295-8.
Lawn ND, Westmoreland BF, Sharbrough FW. Multifocal periodic lateralized epileptiform discharges (PLEDs): EEG features and clinical correlations. Clin Neurophysiol 2000;111:2125-9.
Litt B, Wityk RJ, Hertz SH, Mullen PD, Weiss H, Ryan DD, et al
. Nonconvulsive status epilepticus in the critically ill elderly. Epilepsia 1998;39;1194-202.
Woodford HJ, George J, Jackson M. Non-convulsive status epilepticus: A practical approach to diagnosis in confused older people. Postgrad Med J 2015;91:655-61.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]