Non-convulsive status epilepticus secondary to valproic acid-induced hyperammonemic encephalopathy

Velioğlu, Sibel; Gazioğlu, Sibel

doi:10.1111/j.1600-0404.2006.00793.x

Cited by 38 publications

(15 citation statements)

References 17 publications

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“…Her symptoms and EEG findings immediately improved after administration of VPA was stopped. Therefore, we assessed this episode as VPA-induced non-convulsive status epilepticus (NCSE).The frequency of diagnoses of drug-induced NCSE cases has recently increased, and some patients with NCSE due to VPA-induced hyperammonemic encephalopathy (VHE) have been reported [Velioglu and Gazioglu, 2007]. However, in our case, the serum ammonia concentration was within the normal range; therefore, the cause of the patient's NCSE was probably not VHE.…”

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confidence: 47%

A case of trisomy 18 with exacerbation of seizures triggered by administration of valproic acid

Kobayashi

Ishikawa

Fujii

et al. 2013

American J of Med Genetics Pt A

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We read with interest the article by Kumada et al. [2013] reviewing epilepsy in children with trisomy 18 who remained alive for more than 1 year. We report on and discuss a 2-year-old female patient with trisomy 18 presenting with a unique epilepsy manifestation. She had persistent patent ductus arterious and a ventricular septal defect, which were treated by ligation and pulmonary artery binding, respectively, at the age of 1.5 months. Tonic seizures had occurred as an infant, and she was treated with oral administration of phenobarbital at a previous hospital.She was referred to our hospital at the age of 1 year 7 months due to hepatoblastoma, which was successfully treated by surgical procedures and adjuvant chemotherapy. Upon admission to our hospital, she had epileptic spasms according to ictal EEG findings (Fig. 1A). Interictal EEG showed marked background slowing and repetitive generalized spike/polyspike and wave discharges predominantly over the bilateral frontal areas without typical hypsarrhythmia. Daily administration of valproic acid (VPA) at 11 mg/kg/ day was then begun. However, 4 days after starting VPA, she became stuporous, engaging in intermittent circular rhythmic movements considered to be an automatism. The continuous EEG recording at that point revealed continuous generalized slow spike-wave discharges (Fig. 1B), and intravenous administration of midazolam transiently suppressed the EEG abnormalities (Fig. 1C). Serum liver enzyme (AST and ALT) and ammonia concentrations were within their normal ranges, and the VPA serum level was 30 mg/ml, below the bottom of the reference range (50-100 mg/ml). Brain MRI showed mild brain atrophy (Fig. 1D). Her symptoms and EEG findings immediately improved after administration of VPA was stopped. Therefore, we assessed this episode as VPA-induced non-convulsive status epilepticus (NCSE).The frequency of diagnoses of drug-induced NCSE cases has recently increased, and some patients with NCSE due to VPA-induced hyperammonemic encephalopathy (VHE) have been reported [Velioglu and Gazioglu, 2007]. However, in our case, the serum ammonia concentration was within the normal range; therefore, the cause of the patient's NCSE was probably not VHE. Although patients with some chromosomal disorders have specific manifestations of epilepsy, descriptions of the characteristics of epilepsy and the EEG findings for patients with trisomy 18 are rare. Generally, VPA-induced NCSE is very rare, but it may be necessary to consider it as a possible contributor to trisomy 18-related epilepsy. In this patient, the NCSE has not recurred, but other seizures (tonic seizures and spasms) were refractory to medications including phenobarbital, vitamin B6, clonazepam, clobazam, lamotrigine, topiramate, and thyroid hormone-releasing therapy. We could not perform ACTH therapy because of underlying congenital heart disease and recurrent episodes of infectious disease. Tonic seizures and spasms occurred daily at the age of 2 years.The present case also provides support for the common featu...

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confidence: 47%

A case of trisomy 18 with exacerbation of seizures triggered by administration of valproic acid

Kobayashi

Ishikawa

Fujii

et al. 2013

American J of Med Genetics Pt A

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“…Garg et al [12] reported a patient with neonatal convulsions who presented with VPA-induced hyperammonemiarelated consciousness disturbance and lethargy. Velioğlu et al [13] reported a 19 year-old male with idiopathic generalized epilepsy who exhibited hyperammonemia-induced dizziness, nausea and consciousness disturbance four days after VPA administration. The patient's EEG showed high-voltage sharp waves in the left frontal and temporal regions.…”

Section: Discussionmentioning

confidence: 99%

Valproic Acid Exacerbated Infantile Spasms and Induced Novel Complex Partial Seizures in an Infant with Non-ketotic Hyperglycinemia

Itonaga

Okanari

Korematsu

et al. 2014

E&S

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A male infant who presented with neonatal asphyxia began to exhibit infantile spasms at three months of age. His seizures were refractory to conventional antiepileptic drugs including valproic acid, pyridoxal phosphate, zonisamide, clonazepam and adrenocorticotrophic hormone (ACTH)-Zn. Immediately following re-administration of valproic acid, infantile spasms were exacerbated and novel complex partial seizures with oral automatism and pedaling behaviors appeared. An electroencephalogram showed more severe hypsarrhythmia and novel focal polyspike bursts in the left mid-temporal region. High levels of glycine were detected in the cerebrospinal fluid (CSF) and plasma, and the activity of the glycine cleavage system was partially reduced to 18.0 % (-1.5 SD) in a [1- (13) Case ReportKey words: valproic acid, non-ketotic hyperglycinemia, glycine cleavage system, infantile spasms, complex partial seizures 31 valproic acid exacerbated the basal infantile spasms and induced novel complex partial seizures, suggesting that the patienthad distinctive clinical seizures due to non-ketotic hyperglycinemia.

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“…Seizures may arise from toxic levels of AED (phenytoin > 40 μg/mL, carbamazepine > 18 μg/mL) [24], valproate in patients with inborn errors of metabolism [25], lamotrigine overdose [26], drug interactions during polypharmacy, choice of an inappropriate AED for epilepsy type (eg, carbamazepine with myoclonic epilepsy), or a paradoxical reaction to a correct medication. Withdrawal of the inciting AED is the treatment [24].…”

Section: Medications and Dyesmentioning

confidence: 99%

Treatment of acute and remote symptomatic seizures

Koppel

2009

Curr Treat Options Neurol

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In principle, the use of anticonvulsant drugs does not differ between acute and remote symptomatic seizures, but control of acute symptomatic seizures requires simultaneous treatment of the underlying etiology. Prevention of remote seizures when the risk is known to be high has been the subject of intense efforts at antiepileptogenesis, but the optimal duration of treatment after an injury is not yet known. Appropriate evaluation of a seizure depends on individual circumstances, but findings on examination, laboratory tests (serum electrolytes, magnesium, glucose, assessment of hepatic and renal function), and brain imaging (CT scan or MRI) are necessary to determine the most likely cause. Lumbar puncture is always required when there is suspicion of meningitis or encephalitis. Preferred medications for treatment of acute symptomatic seizures or status epilepticus are those available for intravenous use, such as benzodiazepines, fosphenytoin or phenytoin, valproate, levetiracetam, and phenobarbital. Diazepam is also available as a gel for rectal administration. Seizures that occur in patients with epilepsy because of missed antiepileptic drugs or inadequate serum levels should be treated with additional doses of their regular medications; loading doses can be administered with minimal toxicity in tolerant patients. Surgery is rarely necessary in the acute setting except for intracerebral lesions with rapidly rising intracranial pressure and impending herniation. After seizures are controlled, the provoking condition must also be determined and treated.

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Non-convulsive status epilepticus secondary to valproic acid-induced hyperammonemic encephalopathy

Abstract: In conclusion, although uncommon, a possible induction of non-convulsive status epilepticus by valproate-induced hyperammonemic encephalopathy should be taken into account and properly managed by discontinuation of the drug.

Cited by 38 publications

References 17 publications

A case of trisomy 18 with exacerbation of seizures triggered by administration of valproic acid

A case of trisomy 18 with exacerbation of seizures triggered by administration of valproic acid

Valproic Acid Exacerbated Infantile Spasms and Induced Novel Complex Partial Seizures in an Infant with Non-ketotic Hyperglycinemia

Treatment of acute and remote symptomatic seizures

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