Correspondence: When an article is eligible for submission of
Correspondence, a link to the response form is available within the full-text
article. You must be a
current subscriber who has activated the online portion of your subscription
in order to send a Correspondence. Any reader can read published
Correspondence.
Correspondence to:
ARTICLES:
R.A.B. Badawy, J. M. Curatolo, M. Newton, S. F. Berkovic, and R. A.L. Macdonell
I am writing in reference to the Correspondence by Civardi and Collini
commenting on the paper by Badawy et al. [1] Civardi and Collini base the comments in the Correspondence on previous work carried out in the laboratory for which I am
responsible. Although Civardi was a collaborator on
previous work in the laboratory, neither he nor Collini are currently
involved in research activity in the laboratory. Their Correspondence does not
represent my opinion or that of others working in the laboratory.
References
1. Civardi C, Collini A. Sleep deprivation increases cortical excitability
in epilepsy: syndrome-specific effects [e-online Letter]. Neurology 14 January
2007.
Disclosure: The author reports no conflicts of interest.
Sleep deprivation increases cortical excitability in epilepsy: syndrome-specific effects
14 January 2007
Carlo Civardi, MD, Azienda Ospedaliera “Maggiore della Carità”. Università del Piemonte Orientale “A. Avogadro” C.so Mazzini 18, 28100 Novara, Italy., Alessandra Collini, MD
We read the Badawy et al [1] article with great
interest. The authors described the effects of sleep deprivation (SD) in
normal subjects and in two groups of epileptic patients with idiopathic
generalized (IGE) and focal epilepsy.
In the control group, they reported a
slight increase of cortical excitability due to SD at 250 ms
interstimulus interval (ISI)recovery curve. In epileptic patients,they
cortical excitability increased at short (1, 2, 5, 10 and 15 ms) and long
ISIs (200, 250 and 300 ms). In IGE, these changes were roboust in both
hemispheres, while in focal epilepsy were localized in the seizure focus
hemisphere.
We described consistent and significant
changes in cortical excitability due to SD in normal subjects.[2] To analyze the effects of SD on cortical
excitability, Badawy et al chose a different protocol from ours. They used a round coil
instead of a focal coil and they stimulated the dominant hemisphere in the control group. However, in epileptic patients they considered both.
Badawy et al did not include short ISIs that in our study showed
statistical changes: ISIs 3 and 16 ms. Badawy’s study [1] lasted for 60-90
minutes for each subject while we analyzed a few number of TMS variables
in order to reduce the time of the exam. In such a long period of time, the
variability of cortical excitability could be significant, especially
after 24 hours of SD, thus only ten control stimuli could not be enough.
In addition, we are surprised by specific changes of cortical excitability
related to the epileptic focus. It is known that in epileptic
patients SD "activates EEG" in a specific and diffuse way [3] and in focal
epilepsy TMS discloses a bilateral increase of cortical excitability [4,5]
in a significant number of patients.
The selective activation on
seizure focus hemisphere [1] represents an intriguing but
unexplained finding.
References
1. Badawy RA, Curatolo JM, Newton M, Berkovic SF, Macdonell RA. Sleep
deprivation increases cortical excitability in epilepsy: syndrome-specific
effects. Neurology 2006; 67: 1018-1022.
2. Civardi C, Boccagni C, Vicentini R, et al. Cortical excitability
and sleep deprivation: a transcranial magnetic stimulation study. J Neurol
Neurosurg Psychiatry 2001; 71: 809-812.
3. Rodin E. Sleep deprivation and epileptological implications. In:
Degen R, Rodin EA, eds. Epilepsy, sleep and sleep deprivation. Epilepsy
Res 1991; suppl 2: 265–273.
4. Varrasi C, Civardi C, Boccagni C, et al. Cortical excitability in
drug-naive patients with partial epilepsy. A cross-sectional study.
Neurology 2004; 63: 2051-2055.
5. Cantello R, Civardi C, Cavalli A, et al. Cortical excitability in
cryptogenic localization-related epilepsy: interictal transcranial
magnetic stimulation studies. Epilepsia. 2000; 41: 694-704.
Disclosure: The authors report no conflicts of interst.
Reply from the Authors
14 January 2007
Richard Macdonell, Austin Health Studley Road, Heidelberg, Victoria 3084, Australia, .A.B. Badawy, J. M. Curatolo, M. Newton, S. F. Berkovic
Richard.Macdonell{at}austin.org.au Richard Macdonell, et al.
We thank Civardi et al for their interest in our study [1] and agree that our
study differs in several respects from their study. [2] The primary focus
of our study was to look at changes after sleep deprivation in patients
suffering from epilepsy, rather than in controls.
There may be subtle
changes in excitability in controls that only appear at specific ISI’s,
not included in our study rather than the more robust changes seen in
patients with epilepsy. The 3msec and 16msec ISIs were not ignored but
rather were not included in our experimental paradigms as this was not the
focus.
In response to the comment about unilateral versus bilateral
stimulation in the control group, we relied on previous publications.
[4,6] together with our own unpublished data which indicate that there
are no inter side differences in excitability in a control population
using paired pulse TMS at various interstimulus intervals.
It appears
intuitively unlikely that sleep deprivation causes more excitability in
one hemisphere than another in a control group but this has not yet
been studied. In the IGE group, there was no interside difference in
excitability after sleep deprivation, this only occurred in the focal
group when referenced to the side of seizure focus. There was also no
difference between dominant and non-dominant hemispheres were compared pre
and post sleep deprivation in either epilepsy group.
It is conjecture that using a round coil rather than a figure eight
coil had some impact on the findings. There are no studies to support
this. A round coil is an accepted method of investigating cortical
excitability [7] and interhemispheric asymmetries [8] using TMS.
In any such study, cortical excitability varies over time; one reason
that a much larger group of subjects were included than in the Civardi et
al study. We feel it is unlikely that this explains the differences
between those with focal and generalized epilepsy and controls given the
random order of stimulation at various ISIs.
We agree that sleep deprivation activates the EEG in a specific and
diffuse way, but it is also discriminatory in patients with epilepsy.
Sleep deprivation enhances the probability of detecting specific focal or
generalized EEG abnormalities.[9] Our findings are consistent with this.
We are currently exploring the phenomenon of lateralized excitability in
patients with focal epilepsy in a larger number of patients than in the
references quoted.
References
6. Hamer HM, Reis J, Mueller HH, Knake S, Overhof M, Oertel WH,
Rosenow F. Motor cortex excitability in focal epilepsies not including the
primary motor area-a TMS study. Brain. 2005;128:811-818.
7. Manganotti P, Bongiovanni LG, Fuggetta G, et al. Effects of sleep
deprivation on cortical excitability in patients affected by juvenile
myoclonic epilepsy: a combined transcranial magnetic stimulation and EEG
study. J Neurol Neurosurg Psychiatry 2006;77:56-60.
8. Garry MI Kamen G, Nordstrom MA Hemispheric differences in the
relationship between corticomotor excitability changes following a fine-
motor task and motor learning. J Neurophysiol 2004;91:1570-1578.
9. Leach J P, Stephen L J, Salveta C, Brodie M J. Which
electroencephalography (EEG) for epilepsy? The relative usefulness of
different EEG protocols in patients with possible epilepsy. J Neurol
Neurosurg Psychiatry 2006; 77: 1040-1042.
Disclosure: The authors report no conflicts of interest.