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A year-old male with a prior history of epilepsy presented with focal clonic seizures. His seizures were refractory to multiple anticonvulsants and eventually required pentobarbital coma for 62 days and midazolam coma for 33 days.
Serial brain magnetic resonance imaging MRI showed development of cerebral atrophy at 31 days after admission to our facility and progression of the atrophy at days after admission. This case highlights the development and progression of generalized cerebral atrophy in super refractory status epilepticus. The cerebral atrophy was noticeable at 31 days after admission at our facility which emphasizes the urgency of definitive treatment in patients who present with super refractory status epilepticus.
Further research into direct effects of therapeutic coma is warranted. Introduction Status epilepticus is a neurological emergency with significant morbidity and mortality [ 1 ]. If status epilepticus continues after the induction of anesthesia, it is termed super refractory status epilepticus [ 3 ]. Super refractory status epilepticus itself portends many long-term complications and sequelae now increasingly being recognized [ 3 , 4 ].
Focal cerebral atrophy is a well-known phenomenon after prolonged seizures or status epilepticus. However, global cerebral atrophy is less characterized. Global cerebral atrophy in refractory status epilepticus may be a result of prolonged critical illness, progression of underlying brain pathology causing seizures independent of the status epilepticus, or direct effect of high doses of antiepileptic agents used to treat the status epilepticus [ 4 , 5 ].
Elucidation of pathophysiology and triggers might help in emphasizing clinical paradigms of management that lead to better outcomes.
We present a case of progressive generalized cerebral atrophy in a patient with super refractory status epilepticus treated with prolonged barbiturate coma. Figure 1: Serial brain magnetic resonance imaging MRI. Consecutive fluid attenuated inversion recovery sequences FLAIR of brain MRIs of the patient with super refractory status epilepticus in a medically induced coma.
The serial images show development and progression of diffuse cerebral atrophy. He presented to an outside facility initially with altered mental status, suggestive of a stroke-syndrome, along with focal clonic seizures of his right face along with nystagmus. While at the OSH, he required sequential addition of benzodiazepine, phenytoin, valproic acid, and levetiracetam for his seizures. His seizures were refractory to these therapies, and propofol infusion was started.
He was eventually transferred to our hospital. Ongoing nonconvulsive seizures originating from the left hemisphere were seen on continuous electroencephalography EEG. Due to failure of multiple agents, including propofol, therapeutic barbiturate coma was initiated on the 11th day from status epilepticus onset. He was maintained in a pentobarbital-induced coma for 62 days with multiple failed attempts at weaning.
The maximum rate of the pentobarbital infusion was 7.
The pentobarbital was weaned systematically with first attempt at 24 hours from initiation and then 3 days and 7 days from start of barbiturate coma.
Further attempts were then made during this time as clinically allowed as anticonvulsants were introduced and optimized. Additional anticonvulsants included lacosamide, topiramate, ketogenic diet, phenobarbital level After 62 days on pentobarbital, he developed septic shock requiring vasopressor support and broad spectrum antibiotics.
He was weaned off the pentobarbital and started on midazolam infusion. He remained on midazolam infusion for additional 33 days. Given his past history, there was concern for an undiagnosed metabolic disorder as the etiology for his unclassified epilepsy syndrome. He was started on arginine, carnitine, riboflavin, coenzyme Q10, folinic acid, creatinine, vitamin E, and vitamin C.
He had an extensive workup for the etiology of his status epilepticus.
Plasma amino acids, acylcarnitine, pyruvate, ammonia, and urine acids were obtained and were unremarkable. Mitochondrial DNA screening panel was negative for disease causing mutation. POLG1 sequencing was unremarkable as well as methylmalonic acid, homocysteine, vitamin B12, and sialic acid levels in the urine.
Additionally, testing for fluorescence in situ hybridization FISH , single nucleotide polymorphism SNP array, myotonic dystrophy, Charcot-Marie-Tooth, paraneoplastic panel, and thyroid antibodies were unremarkable. Muscle biopsy showed myopathic changes consistent with his critical illness. Over the course of hospitalization, he had serial MRI brains performed, including an admission MRI at our institution 11 days from onset; Figure 1 b.
Diffuse generalized atrophy was noted in comparison to prior MRI Figure 1 a.
The diffuse cerebral atrophy significantly progressed by 31 days and days from onset of status epilepticus Figures 1 c and 1 d , resp. He eventually was discharged to a long-term acute care facility. On neurological examination prior to discharge, he would spontaneously open his eyes but would not follow commands or track examiner. He would not attempt to speak. He had flaccid quadriparesis.
He required ventilator support. It remained unclear as to the etiology for his refractory status epilepticus.
Arteria cerebral media
Discussion This case illustrates the rapid development and progression of global cerebral atrophy in a patient with super refractory status epilepticus requiring pentobarbital coma for a total of 62 days with 11 days of presumed nonconvulsive seizure activity prior to the definitive treatment with pentobarbital.
A key finding in this case is the development of cerebral atrophy most notably at 31 days and continued progression of the cerebral atrophy at days.In order to visualize the distribution of endogenous peroxisome matrix proteins together with the peroxisomal membrane, we used two-color STED imaging on peroxisomal membranes labeled by anti-PMP70 together with anti-catalase CAT1 or anti-acetyl-CoA acyltransferase1 3-ketoacyl-CoA thiolase, ACAA1 antibodies directed against peroxisomal matrix proteins Fig.
These complications may not be directly related to the medications themselves itself, but rather a reflection of the immobile, critically ill state [ 5 ]. Further attempts were then made during this time as clinically allowed as anticonvulsants were introduced and optimized. Our uniform solution works with any device and operating system and can be easily integrated with a wide range of business apps — Google Drive, Oracle, Salesforce, Office , Egnyte, NetSuite, etc.
Biochemically distinct vesicles from the endoplasmic reticulum fuse to form peroxisomes. Fujiki, Y.