ABSTRACT
BACKGROUND: and purpose: Neuron specific enolase (NSE) is an established biomarker of neuronal damage. It is not clear how much seizures contribute to the neuronal damage, morbidity or mortality in critically ill neurology patients. The aim of this study is to determine the impact of seizures on neuronal injury in critically ill neurology patients by using neuron specific enolase as a biomarker. MATERIAL AND METHODS: Forty patients with clinical evidence of acute central nervous system disease associated with seizures were included as critically ill neurology patients with seizures [CINPS] (age in years 38.8⯱â¯17.54, mean⯱â¯SD; 22 males) and 43 age and sex-matched acute central nervous system disease without seizures were recruited as critically ill neurology patients [CINP] (age in years 37.84⯱â¯17.38 years mean⯱â¯SD; 24 males) The serum NSE assays were performed in CINPS (within 24â¯h of last seizure) and in CINP using an enzyme immunoassay kit. RESULTS: The level of serum neuron specific enolase was significantly higher in CINP with seizures compared to those without seizures. The length of ICU stay was more prolonged in those with seizures. There was a close correlation between the NSE levels and frequency of seizures. There was no significant difference in the mortality between both the groups. CONCLUSIONS: NSE a marker of neuronal injury was elevated in patients with acute central nervous system diseases. It is significantly higher in patients with seizures in comparison to those without seizures. This warrants further studies to document aggressive treatment of seizures in acute neurologically ill patients can reduce neuronal damage.
Subject(s)
Biomarkers/blood , Neurons/pathology , Phosphopyruvate Hydratase/blood , Seizures/blood , Seizures/pathology , APACHE , Adolescent , Adult , Aged , Child , Critical Illness , Female , Glasgow Coma Scale , Hospital Mortality , Humans , Male , Middle Aged , Seizures/mortality , Young AdultSubject(s)
Adaptor Proteins, Signal Transducing/genetics , Lipodystrophy/diagnostic imaging , Lipodystrophy/genetics , Membrane Proteins/genetics , Mutation/genetics , Osteochondrodysplasias/diagnostic imaging , Osteochondrodysplasias/genetics , Subacute Sclerosing Panencephalitis/diagnostic imaging , Subacute Sclerosing Panencephalitis/genetics , Adult , Family Health , Humans , India , Magnetic Resonance Imaging , MaleABSTRACT
BACKGROUND: Subacute sclerosing panencephalitis (SSPE) is a delayed and fatal manifestation of measles infection. Fulminant SSPE is a rare presentation in which the disease progresses to death over a period of 6 months. The clinical features are atypical and can be misleading. CASE REPORT: We report herein a teenage boy who presented with acute-onset gait ataxia followed by right hemiparesis that evolved over 1 month, with left-hemispheric, delta-range slowing on the electroencephalogram (EEG). Magnetic resonance imaging disclosed multiple white-matter hyperintensities, suggesting a diagnosis of acute disseminated encephalomyelitis. He received intravenous steroids, and within 4 days of hospital admission he developed unilateral slow myoclonic jerks. Repeat EEG revealed Rademecker complexes, pathognomonic of SSPE, and an elevated titer of IgG antimeasles antibodies was detected in his cerebrospinal fluid. The disease progressed rapidly and the patient succumbed within 15 days of hospitalization. The diagnosis of SSPE was confirmed by autopsy. CONCLUSIONS: This case illustrates the difficulty of recognizing fulminant SSPE when it manifests with asymmetric clinical and EEG abnormalities.
