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Contingent negative variation in headache.

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BRIEF COMMUNICATIONS
Contingent Negative
Variation in Headache
Alain Maertens de Noordhout, MD,’
Martine Timsit-Berthier, MD,? Meyer Timsit, MD,P
and Jean Schoenen, MD’
Contingent negative variation (CNV), an event-related
slow cerebral potential, was analyzed in 79 consecutive
headache patients. Compared to normal controls (n =
33), CNV did not differ in tension headache (n = 21) or
in combined headaches with a predominant tension
component (n = 13). The mean amplitude of CNV was
significantly (p < 0.001) increased in migraine (n = 29)
as well as in combined headache with predominant migraine (n = 16). All migraineurs were studied between
attacks and without prophylactic treatment. CNV may
be a useful diagnostic test in headache. Its increased
amplitude in migraine might reflect central catecholaminergic hyperactivity.
Maertens de Noordhout A, Timsit-Berthier M,
Timsit M, Schoenen J: Contingent
negative variation in headache.
Ann Neurol 19:78-80, 1986
Contingent negative variation (CNV) is a slow cerebral
potential recorded over the scalp in simple reactiontime tasks with a warning stimulus 116, 17, ,211. It is
thought to be closely modulated by noradrenergic and
dopaminergic systems {9, 14, 191. Its study in headache patients is thus of interest, since central catecholaminergic activity might be enhanced in migraine [6].
Moreover, if CNV undergoes characteristic modifications in migraine, it should be a useful diagnostic
paraclinical test, particularly in combined headache, in
which it is often difficult to determine whether migraine or tension headache prevails. For these reasons,
CNV has been analyzed in 85 consecutive patients
with migraine andor tension headache. Preliminary results of this study have been presented elsewhere {lZ].
Materials and Methods
Case Material and Diagnostic Criteria
Seventy-nine patients were evaluated in this study; 6 of the
original 85 were excluded because of diagnostic uncertainty
or ongoing treatment with @-blockers. None of the remain-
From the *Headache Clinic, Institute of Medicine, HBpital de
BaviPre, University of Liege, Liege, Belgium, and the tLaboratoire
de Neurophysiologie clinique et de Psychopathologie.
Received Mar 25, 1985, and in revised form June 4. Accepted for
publication June 5, 1385.
Address reprint requests to Dr Schoenen, Department of Clinical
Neurophysiology and Neurology, HBpital de Bavigre, BD. Constitution, 66, 4020 Liege, Belgium.
78
ing patients received prophylactic antimigraine drugs, but
they were allowed to take analgesics and/or ergot derivatives.
All rnigrameurs were studied between attacks. Control subjects were recruited among students and the medical staff.
The case material is summarized in the Table.
The diagnostic classifications defined by the World Federation of Neurology-Research Group on Migraine and Headache (1969) were considered in this study. Vahlquist’s [20]
criteria were used for the diagnosis of migraine. Patients with
combined headaches were classified as having “mainly migraine” if they had 2 or more attacks per month, or as having
“mainly tension headaches” if daily pain was their major
complaint and if they experienced fewer than 2 well-defined
migraine attacks per month.
Electrvfihysivlogical Methods
C N V was obtained according to the classic experimencal
model defined by Walter and associates in 1964 1211: the
warning stimulus (S1) was a 50-msec tone followed 1 second
later by a series of 15-Hz flashes that the subject had to
interrupt by pushing a button. Artifact-free CNVs were averaged in six successive sequences of eight trials. The intertrial interval varied randomly between 10 and 30 seconds.
C N V amplitude was measured between pre-S1 baseline and
1,000 msec post-S1 level. The averaged amplitude after 48
trials is the major information reported here.
Results
In the control group (n = 33), mean CNV amplitude
was - 16.8 t 6.0 pV. In patients with tension headache (n = 21), this value was not significantly differ4.14 kV. Patients with combined but
ent: - 15.08
predominantly tension headaches (n = 13) had a mean
CNV amplitude of - 14.97 rfr 6.09 pV, which is not
significantly different from controls. In migraineurs,
mean CNV amplitude was clearly enhanced, -24.78
-+ 6.55 pV in patients with pure migraine (n = 29)
and -27.34
8 kV in patients with combined headaches with predominant migraine (n = 16). These
values were significantly different from either control
group or tension headache group values Cp < 0.001,
Student’s t test). There was no significant difference
between classic and common migraine, nor between
pure migraine and combined headaches with predominant migraine, as shown in Figure 1. Within the two
major diagnostic groups, the CNV parameters considered here did not differ significantly between patients
who were taking analgesics and/or ergot derivatives
and those who were not.
Two illustrative CNV recordings are reproduced in
Figure 2, one from a patient with tension headache,
the other from a migraineur. The six successive CNV
recordings (each being an average of eight trials)
shown in the lower part of this figure demonstrate
another abnormal finding in migraine, lack of habituation. Habituation was reduced in 69% of migraineurs
but in only 19% of patients with tension headache.
*
Case Material
Subjects
Total
Female
Male
Mean
Age (yr)
Controls
Patients
Classic migraine
Common migraine
Combined, mostly
migraine
Combined, mostly
33
79
6
23
16
14
66
5
21
14
19
13
1
2
2
33
41
32.7
34.6
48.8
13
11
2
35.5
21
15
6
38
~
tension
Tension
30r
CNV a w l i t d e
rPCO.OO1
M
--NS-7 7-
O " ' i
'''2"'i
0-i
4s
--
2
--
3
-_
4s
B
A
Fig 2. Examples of contingent negative variation recordings in
tension headache (A) and zn mzgraine (B). (S1 = warning
stimulus; Sz = imperativestimulus.)
10
0
Controls
Tenslon
Cornblned
Combmed
Common
Classic
Tension+
Migraine+
migrame
rnigralne
Fig I . Contingent negative variation (CNV) amplitudes in d$ferent types of headaches. (NS = not signifcant.)
Discussion
The present study demonstrates that CNV amplitude
is increased in migraineurs between attacks and that its
habituation is reduced. Conversely, C N V is normal in
tension headache. There is no influence of analgesics
and ergot derivatives on the CNV parameters studied
here, for no significant differences were observed in
either clinical group between patients taking and those
not taking such drugs. Other pharmacological treatments, however, are able to modify CNV. Our
preliminary data [12) indicate that in migraineurs
P-blockers can normalize CNV values after a 2 to
3-month treatment period. These findings are of
diagnostic and physiopathological interest. Patients frequently are seen with combined headaches. As a complement to the clinical history, CNV may help to determine which type of headache prevails. A high CNV
amplitude would indicate predominance of migraine,
whereas low amplitude suggests that the patient suffers
mainly from tension headaches. The distinction between these two types of headache usually carries therapeutic implications [4, 11).
CNV results from many elementary cerebral activities. The neuronal populations and pathways involved
in its genesis are only partly known [16}. However,
the neurochemical basis of CN V is emerging thanks to
animal experiments 18, 91, pharmacological studies in
humans [lS), studies of mental diseases [l8}, and correlation with neuroendocrine tests 1191. At present,
the following theory can be proposed [lb): norepinephrine and dopamine are major modulators of CNV
by a dual action-they facilitate cholinergic neurons,
which are responsible for slow negative potentials, but
they inhibit y-aminobutyric acid (GABA)-ergic inhibitory interneurons. Increased CN V amplitude can thus
be considered another argument for central catecholaminergic hyperactivity in migraine C2,3, lo}. In addition, it has been shown in animal experiments that
slow negative potentials in the brain are associated
with increased extracellular potassium and cyclic
adenosine monophosphate activity { 131. Extraneuronal
potassium accumulation is also a major feature of
Leiio's spreading depression, thought to be crucial in
the pathogenesis of the migraine attack [l, 3, 5 , 7).
Further studies are needed to determine whether
the modifications of CNV observed in migraineurs are
due to dysfunctioning neurotransmitter systems, abnormal ion fluxes, or both.
~
~~~~~
~
J. Schoenen is a research associate of the National Fund for Scientific
Research (Belgium).
References
1. Amery W K Brain hypoxia: the turning-point in the genesis of
the migraine attack? Cephalalgia 2:83-109, 1982
2. B i g s MJ, Johnson ES: The autonomic nervous system and migraine pathogenesis. In Amery WK, Van Nuetten JM, Wauquier A (eds): The Pharmacological Basis of Migraine Therapy.
London, Pitman, 1984, pp 99-107
Brief Communication: Maertens de Noordhout et al: CNV in Headache 79
3. Bruyn GW: Cerebral cortex and migraine. Adv Neurol
33:151-169, 1982
4. Bruyn GW: The pathomechanism of migraine as a basis for
pharmacotherapy: a clinician epilogue. In Amery WK, Van
Nuetten JM, Wauquier A (eds): The Pharmacological Basis of
Migraine Therapy. London, Pitman, 1984, pp 267-278
5. Gardner-Medwin A k Possible roies of vertebrate neuroglia in
potassium dynamics, spreading depression and migraine. J Exp
Biol 95:111-127, 1981
6. Lance JW, Lambert GA, Goadsby PJ, Duckworth JW: Brainstem influences on the cephalic circulation: experimental data
from cat and monkey of relevance to the mechanism of migraine. Headache 23:258-265, 1983
7. Lauritzen M: Spreading cortical depression in migraine. In
Amery WK, Van Nuetten JM, Wauquier A (eds): The
Pharmacological Basis of Migraine Therapy. London, Pitman,
1984, pp 149-160
8. Libet B: Slow postsynaptic tesponses of sympathetic ganglion
cells as models for slow potential changes in the brain. In Otto
D (ed): Multidisciplinary Perspectives in Event-Related Brain
Potential Research. Washington, DC, U.S. Government Printing Office, 1978, pp 12-19
9. Marczynski TJ: Neurochemical mechanisms in the genesis of
slow potentials: a review and some clinical implications. In Otto
D (ed): Multidisciplinary Perspectives in Event-Related Brain
Potential Research. Washington, DC, U.S. Government Printing Office, 1078, pp 25-35
10. Rose FC: The pathogenesis of a migraine attack. TINS 6:247248, 1983
11. Schoenen J: Place des b6a-bloquants dans le traitement de la
migraine. In Migraine et Cephalkes. Paris, Sandoz, 1984, pp
85-95
12. Schoenen J, Maertens de Noordhout A, Timsit-Berthier M,
Timsit M: Contingent negative variation (CNV) as a diagnostic
and physiopathologic tool in headache patients (abstract). The
Migraine Trust, 5th international symposium, 1984, pp 4 1-42
13. Skinner JE, King G L Contribution of neuronal dendrites to
extracelluar sustained potential shifts. In Kornhuber H H ,
Deecke L (eds): Motivation, Motor and Sensory Processes of
the Brain: Electrical Potentials, Behaviour and Clinical Use.
Amsterdam, Elsevier North Holland, 1980, pp 83-102
14. Skinner JE, Yingling CD: Central gating mechanisms that regulate event-related potentials and behaviour. A neural model for
attention. In Desmedt JE (ed): Attention, Voluntary Contraction and Event-Related Cerebral Potentials (vol 1, Progress in
Clinical Neurophysiology). Basel, Karger, 1977, pp 30-69
15. Thompson JW, Newton P, Pocock PV, et al: Preliminary study
of pharmacology of CNV in man. In Otto D (ed): Multidisciplinary Perspectives in Event-Related Brain Potential Research.
Washington, DC, U.S. Government Printing Office, 1978, pp
51-55
16. Timsit-Berthier M: A propos de I'interprCtation de la variation
contingente negative en psychiatrie. Rev EEG Neurophysiol
11~236-244, 1976
17. Timsit-Berthier M: Les potentiels lents lies aux kv6nernents.
Rev EEG Neurophysiol 6:181-185, 1976
18. Timsit-Berthier M: La VCN et les maladies mentales. Acta
Psychiatr Belg 76:521-550, 1976
19. Timsit-Berthier M, Mantanus H , Marissiaux P, et al: Correlations between the CNV parameters and the neuroendocrine
tesrs. EEG Journal, 1985 (in press)
20. Vahlquist B: Migraine in children. Int Arch Allergy 7:348-355,
1955
21. Walter WG, Cooper R, Aldridge VJ, et al: Contingent negative
variation: an electric sign of sensory-motor association and expectancy in the human brain. Nature (Lond) 203:380-394,
1964
80
Low CSF Protein
Concentration in Idiopathic
Pseudotumor Cerebri
v;jayChandra, MD, PhD,# Srinath N. ~
and Robert J , Anderson, MPH, phD$
~
lM D
l , ~~ ~
An inverse relationship between the cerebrospinal fluid
(CSF) opening pressure and the corresponding protein
value was found for patients with idiopathic pseudotumor cerebri who underwent their first lumbar puncture (LP) prior to the initiation of therapy. This relationship provides evidence for a pressure-dependent bulk
flow absorption for CSF and also suggests that patients
with high CSF pressures will have low CSF protein concentration.
Chandra V, Bellur SN, Anderson RJ: Low CSF
protein concentration in idiopathic pseudotumor
cerebri. Ann Neurol 19:80-82, 1986
Some patients with pseudotumor cerebri have a low
concentration of protein in their lumbar cerebrospinal
fluid (CSF) 12, 4, lo]. However, there is little known
about the importance of the low concentrations. We
conducted a study to determine the implications of the
CSF protein levels in patients with idiopathic pseudotumor cerebri.
Materials and Methods
Diagnosis of idiopathic pseudotumor cerebri was based on
the following criteria: (1) the patient had initial signs and
symptoms of increased intracranial pressure and no evidence
of an encephalopathy; (2) specific radiological tests (e.g.,
pneumoencephalography, ventriculography, arteriography,
or computed tomographic [CT] scans of the head) had excluded a structural lesion; (3) increased intracranial pressure
was documented by a lumbar puncture (LP); ( 4 ) the CSF
composition was normal (i.e., cell count of 5 or less per cubic
millimeter in an uncentrifuged specimen, protein content of
50 mgldl or less, and tests for syphilis negative); and ( 5 ) an
absence of conditions associated with the occurrence of secondary pseudotumor cerebri as summarized by Ahlskog and
ONeill El}. Criteria 1, 2, and 5 were required for diagnosis.
From the "Neuroepidemiology Branch, Intramural Research Program, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, MD, and
the ?Department of Neurology and $Epidemiology-Biometry Program, School of Public Health, University of Illinois at Chicago,
Chicago, IL.
Received Feb 22, 1985, and in revised form June 24. Accepted for
publication July 3, 1985.
Address reprint requests to Dr Chandra, Neuroepidemiology
Branch, NINCDS, N I H Federal Building, Rm 804, 7550 Wisconsin
Avenue, Bethesda, M D 20892.
,
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