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October 2023
Maxim Ioshpa MD

Status epilepticus (SE) is a neurological emergency requiring immediate evaluation and management to prevent significant morbidity or mortality. Previously, status epilepticus was defined as a seizure with a duration equal to or greater than 30 minutes or a series of seizures in which the patient does not regain normal mental status between seizures. The Neurocritical Care Society guidelines from 2012 revised the definition to a seizure with 5 minutes or more of continuous clinical and/or electrographic seizure activity or recurrent seizure activity without recovery between seizures.

Status epilepticus may be convulsive, non-convulsive, focal motor, or myoclonic, and any can become refractory. Convulsive status epilepticus consists of generalized tonic-clonic movements and mental status impairment. Non-convulsive status epilepticus is defined as seizure activity identified on an electroencephalogram with no accompanying tonic-clonic movements. Focal motor status epilepticus involves the refractory motor activity of a limb or a group of muscles on one side of the body with or without loss of consciousness. Refractory status epilepticus refers to continuing seizures (convulsive or non-convulsive) despite appropriate antiepileptic drugs [1].

September 2019
September 2018
Keren Cohen-Hagai MD, Dan Feldman MD, Tirza Turani-Feldman BOT, Ruth Hadary MD, Shilo Lotan MD and Yona Kitay-Cohen MD

Background: Magnesium is an essential intracellular cation. Magnesium deficiency is common in the general population and its prevalence among patients with cirrhosis is even higher. Correlation between serum levels and total body content is poor because most magnesium is intracellular. Minimal hepatic encephalopathy is a subclinical phase of hepatic encephalopathy with no overt symptoms. Cognitive exams can reveal minor changes in coordination, attention, and visuomotor function, whereas language and verbal intelligence are usually relatively spared.

Objectives: To assess the correlation between intracellular and serum magnesium levels and minimal hepatic encephalopathy.

Methods: Outpatients with a diagnosis of compensated liver cirrhosis were enrolled in this randomized, double-blinded study. Patients were recruited for the study from November 2013 to January 2014, and were randomly assigned to a control (placebo) or an interventional (treated with magnesium oxide) group. Serum and intracellular magnesium levels were measured at enrollment and at the end of the study. Cognitive function was assessed by a specialized occupational therapist.

Results: Forty-two patients met the inclusion criteria, 29 of whom were included in this study. Among these, 83% had abnormal cognitive exam results compatible with minimal hepatic encephalopathy. While only 10% had hypomagnesemia, 33.3% had low levels of intracellular magnesium. Initial intracellular and serum magnesium levels positively correlated with cognitive performance.

Conclusions: Magnesium deficiency is common among patients with compensated liver cirrhosis. We found an association between magnesium deficiency and impairment in several cognitive function tests. This finding suggests involvement of magnesium in the pathophysiology of minimal hepatic encephalopathy.

November 2017
Szilvia Szamosi MD, Nóra Bodnár MD, Boglárka Brugós MD, Tibor Hortobágyi MD, Gábor Méhes MD, Zoltán Szabó MD, Edit Végh MD, Ágnes Horváth MD, Zoltán Szekanecz MD, Attila Szűcs MD and Gabriella Szűcs MD
October 2017
Chen Ben David MS, Kassem Sharif MD, Abdulla Watad MD, Nicola Luigi Bragazzi MD MPH PhD and Mohammad Adawi MD MHA
February 2017
Avishay Tzur MD,Yair Sedaka MD, Yariv Fruchtman MD, Eugene Leibovitz, MD, Yuval Cavari MD, Iris Noyman MD, Shalom Ben-Shimol MD, Ilan Shelef MD and Isaac Lazar MD
March 2015
Eilon Krashin MD, Michael Lishner MD, Michal Chowers and Sharon Reisfeld MD
December 2014
Eilon Krashin MD, Michael Lishner MD, Michal Chowers MD and Sharon Reisfeld MD
January 2011
Y. Landau, I. Berger, R. Marom, D. Mandel, L. Ben Sira, A. Fattal-Valevski, T. Peylan, L. Levi, S. Dolberg and H. Bassan

Background: Major advances in the treatment of perinatal asphyxial–hypoxic ischemic encephalopathy followed the translation of hypothermia animal studies into successful randomized controlled clinical trials that substantially influenced the current standard of care.

Objectives: To present our preliminary experience with the first cases of clinical application of therapeutic hypothermia for PA-HIE[1] in what we believe is the first report on non-experimental hypothermia for PA-HIE from Israel.

Methods: We reviewed the medical records, imaging scans, electroencephalograms and outcome data of the six identified asphyxiated newborns who were managed with hypothermia in our services in 2008–2009.

Results: All asphyxiated newborns required resuscitation and were encephalopathic. Systemic hypothermia (33.5ºC) was begun at a median age of 4.2 hours of life (range 2.5–6 hours) and continued for 3 days. All six infants showed a significantly depressed amplitude integrated electroencephalography background, and five had electrographic seizures. One infant died (16%) after 3.5 days. Major complications included fat necrosis and hypercalcemia (n=1), pneumothorax (n=1), and meconium aspiration syndrome (n=2). None of the infants developed major bleeding. Neurodevelopmental follow-up of the five surviving infants at median age 7.2 months (4.1–18.5 months) revealed developmental delays (Battelle screening), with their motor scores ranging from -1 to +1 standard deviation (Bayley scale). None developed feeding problems, oculomotor abnormalities, spasticity or seizures.

Conclusions: Our preliminary experience with this novel modality in a large Tel Aviv neonatal service is consistent with the clinical findings of published trials.






[1] PA-HIE = perinatal asphyxial–hypoxic ischemic encephalopathy


July 2010
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