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ARTICLES: Julio A. Chalela, Ronald L. Wolf, Joseph A. Maldjian, and Scott E. Kasner MRI identification of early white matter injury in anoxic–ischemic encephalopathy Neurology 2001; 56: 481-485 [Abstract] [Full text] [PDF]

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MRI identification of early white matter injury in anoxic–ischemic encephalopathy

I Korn-Lubetzski, "M Sanchez, N Zilber, C Lubetzski, B Zalc"   (16 May 2001)

Reply to Korn-Lubetzki

Julio A Chalela, "Ronald L Wolf, Joseph A Maldjian, Scott E Kasner"   (16 May 2001)

MRI identification of early white matter injury in anoxic–ischemic encephalopathy 16 May 2001
I Korn-Lubetzski Bikur Cholim Hospital Jerusalem and Hopital de la Salpetriere, Paris, "M Sanchez, N Zilber, C Lubetzski, B Zalc" Send Correspondence to journal: Re: MRI identification of early white matter injury in anoxic–ischemic encephalopathy ikl{at}md.huji.ac.il I Korn-Lubetzski, et al.	Chalela et al reported early white matter injury in anoxic-ischemic encephalopathy (AIE) in seven relatively young (median age 31.5 years) patients. (ref. 1) Causes of AIE were various and included patients with cardiac arrest, carbon-monoxide intoxication, or drug abuse. They suggested that the high fatality rate (5/7) might indicate that anoxic white matter injury carries a worse prognosis. (ref. 1) To determine whether demyelination occurs in AIE and could eventually be taken as an initial prognostic factor, we studied prospectively 27 patients with AIE (myocardial infarction and ventricular arrhythmias-85%; respiratory failure or arrest -15 %). Serum level of galactosylceramide, a major component of myelin, has been proved to be a reliable index of demyelination. (ref. 2) Galactosylceramide, undetectable in normal individuals, is detected in sera of patients suffering from MS, stroke or intracranial neoplasm. (ref. 2) All patients had a Glasgow Coma Scale scoring and Galactosylceramide level determination at admission and every second day, until discharge or death. Galactosylceramide levels (initial, maximum and final-within 2 days before death or discharge) were correlated with final outcome, time to death or to discharge, and Glasgow Coma Scale. Twelve patients (6 men, 6 women, mean age 58.9 years) were discharged from the hospital; 15 patients (6 men, 9 women, mean age 58.2 years) died in coma (fatality rate 15/27). Patients who died in coma had a lower mean initial Glasgow Coma Scale score on admission than patients discharged (4.65  1.72 vs 9.42  4.23, p < 0.01). (ref. 3). Positive values of Galactosylceramide (>2.0 nmole/ml) were obtained at least once during the course of hospitalization in 85 % of patients (80% of those who died in coma and 92 % of those discharged - non significant difference). However no significant association was observed between initial, maximal or final Galactosylceramide level and outcome (death while in coma versus discharge), neither between mean level of Galactosylceramide and mean Glasgow Coma Scale score. Demyelination occurs in nearly all cases of anoxic ischemic brain injury, reflecting destruction of the myelin by the metabolic process of hypoxia. Unfortunately, Galactosylceramide level could not be taken as a prognostic indicator. REFERENCES 1. Chalela JA, Wolf RL, Maldjian JA, Kasner SE. MRI identification of early white matter injury in anoxic-ischemic encephalopathy. Neurology 2000; 56: 481-485. 2. Lubetzki C, Thuiller Y, Galli A, et al: Galactosylceramide: a reliable serum index of demyelination in multiple sclerosis. Ann Neurol 1989; 26: 407- 409. 3. Sacco RL, VanGool R, Mohr JP, et al: Non traumatic coma. Glasgow coma score and coma etiology as predictors of 2 weeks outcome. Arch Neurol 1990; 47: 1181-1184.
Reply to Korn-Lubetzki 16 May 2001
Julio A Chalela University of PA School of Medicine, "Ronald L Wolf, Joseph A Maldjian, Scott E Kasner" Send Correspondence to journal: Re: Reply to Korn-Lubetzki chalelaj{at}ninds.nih.gov Julio A Chalela, et al.	We appreciate the comments from Korn-Lubetzki et al. They describe their findings in a small cohort of patients with anoxic encephalopathy in whom galactosylceramide (a surrogate marker of myelin breakdown) was measured. No association was found between galactosylceramide levels and clinical outcome. The authors conclude that demyelination occurs in nearly all patients with diffuse cerebral anoxia but it carries no prognostic significance. The authors only dichotomized the results as either positive or negative, and thus they can only conclude that levels above a threshold of 2 nmole/mL are not associated with worse prognosis. It is possible that very high levels of galactosylceramide may be associated with poor outcome. MRI imaging was not performed in all patients and markers of neuronal injury were not measured, thus the extent of white matter disease and the coexistence of gray matter injury cannot be determined. Elevated levels of galactosylceramide could also result from concomitant spinal cord anoxia. The conclusion that demyelination, as measured only by elevated galactosylceramide levels, is not associated with poor prognosis is therefore not certain. We agree that myelin injury is common in patients with diffuse cerebral anoxia, as this is supported by our findings and by prior CT and MRI studies. The main objective of our study was to determine if myelin injury could occur early after global anoxia. Demyelination is well- recognized in a delayed manner after anoxia but early demyelination has not been previously characterized. We raised the hypothesis that myelinopathy may be a marker of injury severity, but this issue needs to be examined in a larger series including patients who show preferential gray matter involvement and patients who show primarily white matter injury. Nevertheless, before embracing new imaging techniques or biochemical tests, one must bear in mind that the clinical examination is a reliable and time-honored method to assess prognosis in anoxic coma. References: 1. Chalela JA, Wolf RL, Maldjian JA, Kasner SE. MRI identification of early white matter injury in anoxic-ischemic encephalopathy. Neurology 2001; 56: 481-485. 2. Lubetzki C, Thuiller Y, Galli A, et al. Galactosylceramide: a reliable serum index of demyelination in multiple sclerosis. Ann Neurol 1989: 26: 407-409. 3. Sacco RL, VanGool R, Mohr JP, et al. Non-traumatic coma. Glasgow coma score and coma etiology as predictors of 2- week outcome. Arch Neurol 1990; 47: 1181-1184.