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Electroconvulsive therapy and brain lipids.

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Electroconvulsive Therapy
and Brain Lipids
John A. Detre, M D
In their recent report Woods and Chiu 111 set out to use in
vivo ‘H magnetic resonance spectroscopy (MRS) to study
alterations in brain lactate produced by electroconvulsive
therapy (ECT). Instead, the authors concluded that ECT
treatments produce alterations in “brain lipids” based on difference spectra obtained before and after ECT therapy.
It is surprising that no lactate resonance was demonstrated
anywhere in the paper. Several authors have successfully obtained lactate measurements from human brain using ‘H
MRS 12-41; however, doing so requires sufficient spatial localization to exclude contamination from subcutaneous and
cranial fat. Figure 2 in the article by Woods and Chiu shows
two spectra obtained before and after ECT (B and C). Both
contain broad lipid resonances which appear 90 degrees out
of phase with the NAA resonance. Since it is widely accepted
that, at least in normal brain, little or no fat resonance is
detected using ‘H MRS, it is likely that the observed lipid
signal is due to contamination from outside the VOI. This
lipid signal obscures the underlying lactate resonance. Some
mention is made in the paper of lactate editing experiments,
but these results are not shown.
The authors attempt to demonstrate an increase in lactate
by subtracting spectra obtained before and after ECT. While
difference spectroscopy is a commonly used technique, it is
valid only when both spectra are obtained under identical
conditions, generally in immediate succession. Since it would
be impossible to perform ECT inside a high-field magnet,
these conditions clearly cannot be met. Small variations in
coil tuning, loading, or magnetic field homogeneity could
easily account for the differences in fat contamination observed.
The authors exclude fat contamination by stating that the
lipid signal increased in 5 successive patients. Although this
may have been the case, in Figures 2, 3, and 4 “difference”
spectra are shown with random phasing of the NAA resonance, making it difficult to determine whether the difference was, in fact, positive or negative. Since the NAA resonance was used for phasing the spectra, it is hard to
understand why the phase should not be the same in all
spectra. Furthermore, the areas under the lipid peaks in the
difference spectra appear t o be an order of magnitude greater
than the NAA, suggesting a “brain lipid” concentration of
100 mM, several orders of magnitude greater than free fatty
acid concentrations measured in mammalian brain after
bicuculline-induced seizures 153.
While in vivo ‘H MRS offers a potentially powerful window into human brain metabolism, it is technically demanding and susceptible to artifact. The data presented by
Woods and Chiu fail to address their original question and
do not clearly support their conclusions.
Department of Nearology
Hospital of the Univenity of Penruylvania
Philadehhiu, P A
1. Woods BT, Chiu T-M. In vivo ‘H spectroscopy of the human
brain following electroconvulsive therapy. Ann Neurol 1990;
2. Bruhn H, FrahmJ, Gyngell ML, et al. Noninvasive differentiation
of tumors with use of localized H-1 MR spectroscopy in vivo:
initial experience in patients with cerebral tumors. Radiology
3. Hanstock CC, Rothman DL, Prichard JW, et al. Spatially localized
‘H NMR spectra of metabolites in the human brain. Proc Natl
Acad Sci USA 1988;85:1821-1825
4. Detre JA, Wang 2, Bogdan AR, et al. Regional variation in brain
lactate in Leigh syndrome by localized ‘H magnetic resonance
spectroscopy. Ann Neurol 1991;29:218-221
5. Siesjo BK, Ingvar M, Westerberg E. The influence of bicuculline-induced seizures on free fatty acid concentrations in cerebral cortex, hippocampus, and cerebellum. J Neurochem
Bryan T. Woods, MD, and Tak-Ming Chin, PhD
In response to Dr Detre’s objection rhar no lactate resonance
was demonstrated, we did see a small lactate signal in 2 patients after electroconvulsive therapy (ECT), and have so
noted in our paper {If.
Whereas it is generally accepted that one sees little or no
lipid signal in normal brain at long T E s , a readily identifiable
lipid signal has been detected in normal brain at the short TE
we used in our studies E2). In any case, we do not consider
that human brains studied 1 hour after ECT are “normal,”
and the whole point of our paper was that the major effect
of ECT was a marked quantitative increase in the brain lipid
signal. As to the likelihood of inadvertent contamination, it
would have to take place on only those scans done after ECT,
and never on the ones done before, and we have now made
this same lipid signal observation in 8 separate patients. Of
a total of 43 separate scans, 17 of which were done within
90 minutes of ECT, and 26 done either before or more than
36 hours after ECT, we have no failures of the lipid signal to
increase shortly after ECT in comparison to control studies
in the same patients.
Dr Detre seems to misunderstand the subtraction technique. It is well known that in difference spectroscopy {3],
a residual peak resembling a derivative signal may result from
subtraction of two peaks with identical amplitudes but
slightly different phase and frequency. Subtraction errors of
this kind may be due to spectrometer stability and are relatively common. In any case, incomplete subtraction of the
N-AA peak before and after ECT would not, in itself, generate a lipid signal at a different position in the ‘H spectrum.
Furthermore, one should not compare the area under the
lipid peak to the area under the N-AA peak in the difference
spectra, as Dr Detre suggests, because the N-AA peak is in
large part subtracted out.
We indicated in our paper [1f that in 1 of the studies the
maximum lipid to N-AA area ratio was 3.75. In interpreting
this it should be recalled that the area under a magnetic
resonance spectroscopy (MRS) peak is determined by the
number of molecules times the number of protons per molecule. Thus free fatty acids (FFA) are likely to have 30 to 40
and diacylglycerol (DAG) 60 to 80 resonant protons per
Copyright 0 1991 by the American Neurological Association 429
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electroconvulsive, brain, therapy, lipid
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