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DOI 10.1212/01.WNL.0000163991.97456.03
2005;64;1879-1883Neurology
G. L. Krauss, A. Abdallah, R. Lesser, et al.
misdiagnosed with epilepsy
Clinical and EEG features of patients with EEG wicket rhythms
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® is the official journal of the American Academy of Neurology. Published continuouslyNeurology
Clinical and EEG features of patients with
EEG wicket rhythms misdiagnosed
with epilepsy
G.L. Krauss, MD; A. Abdallah, BA; R. Lesser, MD; R.E. Thompson, PhD; and E. Niedermeyer, MD
Abstract—Background: EEG wicket rhythms are 6- to 11-Hz medium-to-high voltage bursts that are sometimes misiden-
tified as epileptogenic activity. The authors determined the clinical and EEG features of patients with wicket rhythms
who had been incorrectly diagnosed with epilepsy. Methods: Electroencephalographers at an epilepsy center re-read EEGs
for patients referred for epilepsy management and identified patients with wicket rhythms. On further evaluation, the
majority (54%; 25/46) of these patients were found not to have epilepsy. The authors compared the clinical and EEG
features for the 25 patients with wickets and nonepileptic episodes with those of age- and sex-matched patients with
partial-onset epilepsy using univariate and multivariate analysis. Results: Several features distinguished patients with
EEG wicket patterns and nonepileptic episodes (n ϭ 25) from age- and sex-matched patients with epilepsy (n ϭ 25):
mid-adult age at onset of episodes (mean 38.4 years vs 19.8 years), prolonged clinical episodes (mean 155 minutes vs 2.3
minutes), and long duration of EEG wicket patterns (mean 0.66 seconds vs 0.11 second spikes). After controlling for other
factors, patients without major confusion during episodes were unlikely to have epilepsy. Conclusion: Wicket patterns are
often interpreted as epileptogenic. This distinctive EEG pattern should be considered in patients with clinical episodes
atypical for epilepsy.
NEUROLOGY 2005;64:1879–1883
Patients with nonepileptic episodes may be misdiag-
nosed as having epilepsy when EEG wicket rhythms
are misinterpreted as interictal spikes and sharp
waves.1
Wicket rhythms are “normal variant” 6- to
11-Hz medium-to-high voltage EEG bursts that have
no epileptogenic potential.2,3
We determined the fea-
tures of clinical episodes and EEG that distinguished
patients with nonepileptic episodes and EEG wicket
patterns from patients with partial-onset epilepsy
and epileptogenic activity on EEG. Patients might
avoid delayed diagnosis and unnecessary exposure to
antiepilepsy drugs if neurologists more accurately
discriminate between wicket patterns and epilepto-
genic activity.
Methods. Patients previously diagnosed with epilepsy were
evaluated at the Johns Hopkins outpatient epilepsy clinic. Pa-
tients’ previous EEG tracings were obtained from other EEG
laboratories and “blindly” re-read by Johns Hopkins electroen-
cephalographers (G.L.K. or R.P.L.). During a 6-year period (Janu-
ary 1996 to December 2002), we evaluated 2,274 new patients; 46
patients had previous EEG available and had EEG wicket pat-
terns. The patients with EEG wicket patterns had been diagnosed
with epilepsy prior to their Johns Hopkins visit. Twenty-one of the
patients with wicket patterns also had epileptogenic patterns on
the previously performed EEGs or had seizures confirmed with
prolonged video EEG monitoring. The remaining 25 (54%) pa-
tients had EEG wicket patterns, but no true spikes or sharp
waves, on previous EEGs and had nonepileptic episodes. We per-
formed one-to-one matching of these 25 “wicket” patients with
patients with partial seizures based on age at date of EEG (Ϯ3
years) and sex. Partial-seizure disorders were confirmed by the
epileptogenic patterns on EEG or video-EEG (interictal spikes and
sharp waves or rhythmic ictal patterns). For both patients and
matches, we collected demographic information, a description of
patients’ clinical episodes (precipitants, duration, presence of pro-
dromal symptoms, presence of confusion and motor signs) and
EEG findings characteristic of wicket and interictal spikes and
sharp waves (frequency, amplitude, duration). Clinical informa-
tion, such as seizure etiology and MRI, was collected via chart
review and an extensive questionnaire. The presence of head
trauma was defined as a history of major head injury (e.g., skull
fracture, cerebral contusion on imaging) or trauma causing loss of
consciousness.
All statistical analyses were performed using the STATA 7.0
statistical software package. Simple descriptive statistics and uni-
variate analyses were performed on the clinical and demographic
variables in the data set. Simple t tests with the Bonferroni cor-
rection for multiple measures were used to compare mean differ-
ences between symptoms and signs for wicket and epileptic
patients for the continuous variables. Outcome data that were
skewed, such as episode duration, were log transformed. Because
of a low sample size, Fisher exact test was used to compare cate-
gorical and dichotomous outcomes between wicket and epileptic
patients. Since the data were clustered by case-control pairs, con-
ditional logistic regression was used in the multivariate analysis.
The conditional logistic regression analysis could not be performed
for models that contained outcomes with no variability within
matched case-control clusters. In these cases, the Huber–White
sandwich estimator of variance along with clustering of observa-
tions within case-control cohorts was used.4
Results. Twenty-five of 46 patients (54%) had wicket
rhythms misinterpreted as epileptogenic activity; all of
these 25 patients had nonepileptic clinical episodes. The 25
patients with wicket patterns and nonepileptic episodes
typically developed clinical episodes in mid-life: mean 38.4
years (95% CI: 32.5, 44.3) compared to late teen and early
adult years for matched patients with complex partial sei-
From the Departments of Neurology (Drs. Krauss, Lesser, and Niedermeyer, and A. Abdallah) and Biostatistics (Dr. Thompson), School of Public Health,
Johns Hopkins University, Baltimore, MD.
Received December 3, 2004. Accepted in final form March 3, 2005.
Address correspondence and reprint requests to Dr. Gregory Krauss, Meyer 2-147, 600 N. Wolfe St., Baltimore, MD 21287; e-mail: gkrauss@jhmi.edu.
Copyright © 2005 by AAN Enterprises, Inc. 1879
zures: mean 19.8 years (13.6, 25.9), p Ͻ 0.0001 (table 1).
The clinical episodes for the patients with wicket rhythms
were much longer in duration (mean 155.8 minutes) com-
pared to patients with complex partial seizures (mean 2.4
minutes; log duration, p Ͻ 0.01). The average frequency of
patients’ clinical episodes was similar for patients with
wickets (mean 21 per year [0.43, 42.6]) and patients with
complex partial seizures (mean 23.7 seizures per year [2.1,
45.2]; p ϭ 0.9). The duration of wicket rhythm bursts were
longer (mean 0.66 seconds [0.5, 0.8]) compared to interictal
epileptogenic patterns (mean 0.11 seconds [0.09, 0.12]; p Ͻ
0.001). EEG frequencies were similar between wicket and
interictal epileptogenic patterns, with a slightly slower fre-
quency for wicket rhythms (9.3 Hz [8.35, 10.21]) compared
to interictal epileptogenic patterns (10.8 Hz [9.7, 12]; p ϭ
0.05).
There was considerable heterogeneity in clinical symp-
toms across patients in both groups (table 2). Signs and
symptoms that differed between patients with wicket pat-
terns and patients with seizures were as follows: sensory
symptoms (mostly limb paresthesias) were uncommon in
patients with epilepsy, while patients with partial-onset
seizures were much more likely to have confusion and oral
automatisms. Fainting symptoms occurred only in patients
with wicket patterns. Both groups frequently reported con-
fusion and histories of head trauma. Patients who experi-
enced confusion, however, were 10 to 40 times more likely
to have epilepsy after controlling for other covariates. This
result is significant in models that control for age at symp-
tom onset and EEG frequency or EEG frequency alone,
and approaches significance when controlling for age at
onset alone. The majority (52%) of patients with epilepsy
had abnormal MRI (most commonly hippocampal atrophy,
low grade tumor, encephalomalacia) compared to 16% of
patients with wicket rhythms (nonspecific white matter
changes, one subarachnoid cyst).
An increase in the age at onset resulted in a decreased
likelihood of having epilepsy, with a predicted OR of ap-
Table 1 Clinical and EEG characteristics for patients with wicket patterns and epilepsy
Wicket patients Epilepsy patients p Value
Female, % 84.0 72.0
Head trauma, % 28.0 24.0
Log (episode duration), min 2.36 (1.22, 3.50) 0.50 (0.18, 0.83) 0.0013*
Episode frequency/y 21.50 (0.43, 42.57) 23.65 (2.13, 45.17) 0.8835
EEG duration, s 0.66 (0.52, 0.81) 0.11 (0.09, 0.12) Ͻ0.0001
EEG frequency, Hz 9.28 (8.35, 10.21) 10.84 (9.70, 11.98) 0.0486
MRI, %
Abnormal 16.0 52.0 0.025†
Normal 60.0 36.0
No MRI 24.0 12.0
Values are % or mean (95% CI). p Values from the t test.
* The natural log was included, since episode duration was highly skewed.
† p Value from Fisher exact test.
Table 2 Symptoms and signs for patients with wicket activity and epilepsy
Variable Wicket patients, n ϭ 25 Epilepsy patients, n ϭ 25 p Value*
Motor activity 0.0 20.0 0.050
Confusion 56.0 96.0 0.001*
Psychic 20.0 4.0 0.189
Sensory 56.0 4.0 Ͻ0.001*
Oral automatisms 0.0 40.0 0.001*
Nausea 16.0 0.0 0.110
Staring 4.0 24.0 0.098
Fainting 32.0 0.0 0.004*
Shaking 20.0 0.0 0.050
Weakness 20.0 0.0 0.050
Speech arrest 0.0 12.0 0.235
Vomiting 8.0 0.0 0.490
Aura prior 12.0 40.0 0.051
Other Rapid breathing, decreased
ability to concentrate, burning
sensation, headache
Collapse, activity arrest, olfactory
aura, wandering
Group differences are evaluated by Fisher exact test. Values are %.
* Significant with Bonferroni correction for multiple measures.
1880 NEUROLOGY 64 June (1 of 2) 2005
proximately 0.9 for every year increase in the age at onset
(figure 1). This is significant (p ϭ 0.001) after controlling
for confusion and EEG frequency.
Patients often had single discharges or brief bursts of
wicket activity that appeared morphologically similar to
interictal spikes and sharp waves (figure 2, A and B). All
patients with wicket activity, however, also had long focal
runs of semirhythmic 6- to 11-Hz activity that contained
wickets and distinguished their EEG from interictal spikes
and sharp waves and ictal EEG patterns (figure 3, A and
B). EEG waveform durations greater than 0.26 seconds
indicated a wicket pattern with a corresponding 100% sen-
sitivity and specificity for this clinical group.
Discussion. Epilepsy was incorrectly diagnosed in
a group of patients with clinical episodes that were
atypical for seizures; the misinterpretation of EEG
wicket patterns contributed to patients’ misdiagno-
sis. While this is a retrospective study, the case-
control findings provide clinical clues that may help
clinicians distinguish patients with nonepileptic epi-
sodes and wicket patterns from patients with
epilepsy.
EEG wicket patterns are usually benign and do
not suggest the presence of epilepsy.5
Within a single
EEG recording, wickets may range in appearance
from single sporadic spikes to trains of arciform dis-
charges.6
Trains of wicket activity typically have a
crescendo-decrescendo envelope and can often be
found bilaterally over temporal regions, though not
necessarily on both sides at the same time. Single
wicket spikes are those that are commonly misinter-
preted as temporal spikes or sharp waves due to
their similarity in appearance.6
Interictal spikes and
sharp waves often have a following slow wave that
distinguishes them from isolated wickets. In our se-
ries, patients with brief wicket patterns that might
be mistaken for interictal spikes and sharp waves
also had long runs of 6- to 11-Hz semirhythmic activ-
ity over the same temporal regions. Interictal spikes
and sharp waves were all brief in duration for our
patient sample (Ͻ0.26 seconds), a factor that distin-
guished patients with partial seizures from those
with wickets. Occasionally, patients with partial sei-
zures may have longer duration bursts of focal epi-
leptogenic activity (spikes, sharp waves, and
paroxysmal slowing).
Wicket patterns are most common in people over
age 33 years7
; this is in accordance with the mid-
adult age at onset of episodes seen in the nonepilep-
tic group in this study. It has been reported that
wicket activity may be associated with cerebrovascu-
lar disease in some patients,8
however, this associa-
tion has not been confirmed in controlled studies and
is most commonly reported in patients with EEG
wickets and focal slowing (“minor sharp and slow
pattern”).3,9,10
Wicket activity has been classified as a
normal variant EEG pattern. This term is meant to
Figure 1. Distribution of age at onset of clinical episodes
(n ϭ 25 for each group).
Figure 2. (A) Wicket activity in
a patient with episodic dizzi-
ness. There is rhythmic 6-Hz
activity, which occurs in brief
bursts and longer trains. This
wicket activity is maximal over
the left temporal area, but was
also present on the right. The
patient has a history of a right
cerebrovascular accident. (B)
Right temporal sharp wave in a
patient with complex partial
seizures and MRI evidence of
right mesial temporal sclerosis.
Unlike the wicket activity, the
sharp wave occurs in isolation
without a buildup of arciform
waveforms.
June (1 of 2) 2005 NEUROLOGY 64 1881
help de-emphasize an association between wicket ac-
tivity and epilepsy.
Following evaluation at our epilepsy clinic, study
patients initially diagnosed with epilepsy were found
to have alternative diagnoses, most commonly near-
syncope, psychogenic nonepileptic seizures, anxiety,
hyperventilation, migraine, or postconcussive syn-
dromes. Many patients had typical symptoms of syn-
cope or near-syncope: postural light-headedness or
unconsciousness, slumping or falling, occasional
stiffening or jerking but no full convulsions, pale-
ness, and nausea.11,12
Many patients also had nonepi-
leptic psychogenic seizures with features atypical for
seizures, such as retained alertness despite bilateral
motor signs and repeated sensory episodes lasting
more than 4 minutes.13
These symptoms should sug-
gest the possibility of diagnoses other than epilepsy
when they occur.
A limitation of this study is the retrospective de-
sign and the limited sample size. During rereading of
previous EEGs, records may have been classified as
showing wicket activity rather than sharp waves or
spikes based on patients’ atypical clinical presenta-
tions. Wicket activity and epileptogenic activity,
however, were confirmed on readings of additional
EEG, with the electroencephalographer blinded to
the clinical history and previous EEG findings.
Moreover, 46% of patients with wicket activity also
had spikes and sharp waves on their previous and
Johns Hopkins University EEGs. These patients
were confirmed to have epilepsy. Finally, the referral
population from which the patients for this study
were chosen is a limitation.
Neurologists often noted in their consultations
that they were uncertain of the etiology of patients’
clinical episodes due to their atypical features; nev-
ertheless, they subsequently relied on incorrect EEG
interpretations in making a diagnosis of epilepsy.
Nonepileptic conditions are frequently misdiagnosed
as epilepsy and this error can lead to many prob-
lems, such as frustration for the patient when the
misdiagnosis is realized, a delay in appropriate diag-
nosis and treatment, and inappropriate treatment
with antiepileptic drugs.11,14
Several patients were
unnecessarily exposed to antiepileptic drugs for 2 or
more years. Antiepileptic drugs are costly and pa-
tients without epilepsy need not tolerate the side
effects of such drugs, which are unlikely to control
their episodes.15
Although the EEG is a useful diagnostic test for
epilepsy, incorrect interpretations may lead to incor-
rect diagnoses. While spikes and sharp waves are
relatively specific for epilepsy, they are sometimes
difficult to identify correctly: some patterns, includ-
ing wickets, appear similar in appearance to interic-
tal epileptogenic activity. Physicians should be
cautious in diagnosing epilepsy in the presence of
atypical clinical episodes combined with uncertain
EEG findings.16
A useful clinical technique for deter-
mining whether brief arciform transients are actu-
ally fragments of a wicket rhythm is to see whether
similar but prolonged wicket rhythms are present
elsewhere in the EEG (see figure 3, A and B). Some
patients may benefit from additional EEG recording
to see whether brief transients are components of a
wicket rhythm or, conversely, to see if true spikes
and sharp waves might appear. A better understand-
ing of normal variant patterns such as wickets is
crucial to the prevention of epilepsy misdiagnosis.8
Figure 3. There is a brief burst of wicket activity in the left and right temporal leads (A). Six seconds later, there is more
prolonged wicket activity (B), which is recorded maximally over the left temporal lobe. The more prolonged wicket activity
helps distinguish the brief bursts of wicket activity from interictal spikes and sharp waves.
1882 NEUROLOGY 64 June (1 of 2) 2005
References
1. Benbadis SR, Tatum WO. Overinterpretation of EEGs and misdiagnosis
of epilepsy. J Clin Neurophysiol 2003;20:42–44.
2. Westmoreland BF. Epileptiform electroencephalographic patterns.
Mayo Clin Proc 1996;71:501–511. Review.
3. Asokan G, Pareja J, Niedermeyer E. Temporal minor slow and sharp
EEG activity and cerebrovascular disorder. Clin Electroencephalogr
1987;18:201–210.
4. StataCorp 2001. Stata Statistical Software. Release 7.0. Vol 1. College
Station, TX: Stata Corporation, 2001;209.
5. Klass DW, Westmoreland BF. Nonepileptogenic epileptiform electroen-
cephalographic activity. Ann Neurol 1985;18:627–635.
6. Reiher J, Lebel M. Wicket spikes: clinical correlates of a previously
undescribed EEG pattern. Can J Neurol Sci 1977;4:39–47.
7. Batista MS, Coelho CF, de Lima MM, Silva DF. A case-control study of
a benign electroencephalographic variant pattern. Arq Neuropsiquiatr
1999;57:561.
8. Kellaway P. Orderly approach to visual analysis: elements of the nor-
mal EEG and their characteristics in children and adults. In: Ebersole
JS, Pedley TA, eds. Current practice of clinical electroencephalography,
3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2003;127–132.
9. Bruens JH, Gastaut H, Giove G. Electroencephalographic study of the
signs of chronic vascular insufficiency of the Sylvian region in aged
people. Electroencephalogr Clin Neurophysiol 1960;12:283–295.
10. Koshino Y, et al. Temporal minor slow and sharp activity in psychiatric
patients. Clin Electroencephalogr 1990;21:225–232.
11. Smith D, et al. The misdiagnosis of epilepsy and the management of
refractory epilepsy in a specialist clinic. QJM 1999;92:15–23.
12. Bergfeldt L. Differential diagnosis of cardiogenic syncope and seizure
disorders. Heart 2003;89:353–358.
13. Fleisher W, et al. Comparative study of trauma-related phenomena in
subjects with pseudoseizures and subjects with epilepsy. Am J Psychia-
try 2002;159:660–663.
14. Scheepers B, Clough P, Pickles C. The misdiagnosis of epilepsy: find-
ings of a population study. Seizure 1998;7:403–406.
15. Chadwick D, Smith D. The misdiagnosis of epilepsy. BMJ 2002;324:
495–496.
16. Worrell GA, Lagerlund TD, Buchhalter JR. Role and limitations of
routine and ambulatory scalp electroencephalography in diagnosing
and managing seizures. Mayo Clin Proc 2002;77:991–998. Review.
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June (1 of 2) 2005 NEUROLOGY 64 1883
DOI 10.1212/01.WNL.0000163991.97456.03
2005;64;1879-1883Neurology
G. L. Krauss, A. Abdallah, R. Lesser, et al.
with epilepsy
Clinical and EEG features of patients with EEG wicket rhythms misdiagnosed
This information is current as of June 13, 2005
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Clinical and eeg features of patients with eeg wicket rhythms misdiagnosed with epilepsy

  • 1. DOI 10.1212/01.WNL.0000163991.97456.03 2005;64;1879-1883Neurology G. L. Krauss, A. Abdallah, R. Lesser, et al. misdiagnosed with epilepsy Clinical and EEG features of patients with EEG wicket rhythms This information is current as of June 13, 2005 http://www.neurology.org/content/64/11/1879.full.html located on the World Wide Web at: The online version of this article, along with updated information and services, is 0028-3878. Online ISSN: 1526-632X. since 1951, it is now a weekly with 48 issues per year. Copyright . All rights reserved. Print ISSN: ® is the official journal of the American Academy of Neurology. Published continuouslyNeurology
  • 2. Clinical and EEG features of patients with EEG wicket rhythms misdiagnosed with epilepsy G.L. Krauss, MD; A. Abdallah, BA; R. Lesser, MD; R.E. Thompson, PhD; and E. Niedermeyer, MD Abstract—Background: EEG wicket rhythms are 6- to 11-Hz medium-to-high voltage bursts that are sometimes misiden- tified as epileptogenic activity. The authors determined the clinical and EEG features of patients with wicket rhythms who had been incorrectly diagnosed with epilepsy. Methods: Electroencephalographers at an epilepsy center re-read EEGs for patients referred for epilepsy management and identified patients with wicket rhythms. On further evaluation, the majority (54%; 25/46) of these patients were found not to have epilepsy. The authors compared the clinical and EEG features for the 25 patients with wickets and nonepileptic episodes with those of age- and sex-matched patients with partial-onset epilepsy using univariate and multivariate analysis. Results: Several features distinguished patients with EEG wicket patterns and nonepileptic episodes (n ϭ 25) from age- and sex-matched patients with epilepsy (n ϭ 25): mid-adult age at onset of episodes (mean 38.4 years vs 19.8 years), prolonged clinical episodes (mean 155 minutes vs 2.3 minutes), and long duration of EEG wicket patterns (mean 0.66 seconds vs 0.11 second spikes). After controlling for other factors, patients without major confusion during episodes were unlikely to have epilepsy. Conclusion: Wicket patterns are often interpreted as epileptogenic. This distinctive EEG pattern should be considered in patients with clinical episodes atypical for epilepsy. NEUROLOGY 2005;64:1879–1883 Patients with nonepileptic episodes may be misdiag- nosed as having epilepsy when EEG wicket rhythms are misinterpreted as interictal spikes and sharp waves.1 Wicket rhythms are “normal variant” 6- to 11-Hz medium-to-high voltage EEG bursts that have no epileptogenic potential.2,3 We determined the fea- tures of clinical episodes and EEG that distinguished patients with nonepileptic episodes and EEG wicket patterns from patients with partial-onset epilepsy and epileptogenic activity on EEG. Patients might avoid delayed diagnosis and unnecessary exposure to antiepilepsy drugs if neurologists more accurately discriminate between wicket patterns and epilepto- genic activity. Methods. Patients previously diagnosed with epilepsy were evaluated at the Johns Hopkins outpatient epilepsy clinic. Pa- tients’ previous EEG tracings were obtained from other EEG laboratories and “blindly” re-read by Johns Hopkins electroen- cephalographers (G.L.K. or R.P.L.). During a 6-year period (Janu- ary 1996 to December 2002), we evaluated 2,274 new patients; 46 patients had previous EEG available and had EEG wicket pat- terns. The patients with EEG wicket patterns had been diagnosed with epilepsy prior to their Johns Hopkins visit. Twenty-one of the patients with wicket patterns also had epileptogenic patterns on the previously performed EEGs or had seizures confirmed with prolonged video EEG monitoring. The remaining 25 (54%) pa- tients had EEG wicket patterns, but no true spikes or sharp waves, on previous EEGs and had nonepileptic episodes. We per- formed one-to-one matching of these 25 “wicket” patients with patients with partial seizures based on age at date of EEG (Ϯ3 years) and sex. Partial-seizure disorders were confirmed by the epileptogenic patterns on EEG or video-EEG (interictal spikes and sharp waves or rhythmic ictal patterns). For both patients and matches, we collected demographic information, a description of patients’ clinical episodes (precipitants, duration, presence of pro- dromal symptoms, presence of confusion and motor signs) and EEG findings characteristic of wicket and interictal spikes and sharp waves (frequency, amplitude, duration). Clinical informa- tion, such as seizure etiology and MRI, was collected via chart review and an extensive questionnaire. The presence of head trauma was defined as a history of major head injury (e.g., skull fracture, cerebral contusion on imaging) or trauma causing loss of consciousness. All statistical analyses were performed using the STATA 7.0 statistical software package. Simple descriptive statistics and uni- variate analyses were performed on the clinical and demographic variables in the data set. Simple t tests with the Bonferroni cor- rection for multiple measures were used to compare mean differ- ences between symptoms and signs for wicket and epileptic patients for the continuous variables. Outcome data that were skewed, such as episode duration, were log transformed. Because of a low sample size, Fisher exact test was used to compare cate- gorical and dichotomous outcomes between wicket and epileptic patients. Since the data were clustered by case-control pairs, con- ditional logistic regression was used in the multivariate analysis. The conditional logistic regression analysis could not be performed for models that contained outcomes with no variability within matched case-control clusters. In these cases, the Huber–White sandwich estimator of variance along with clustering of observa- tions within case-control cohorts was used.4 Results. Twenty-five of 46 patients (54%) had wicket rhythms misinterpreted as epileptogenic activity; all of these 25 patients had nonepileptic clinical episodes. The 25 patients with wicket patterns and nonepileptic episodes typically developed clinical episodes in mid-life: mean 38.4 years (95% CI: 32.5, 44.3) compared to late teen and early adult years for matched patients with complex partial sei- From the Departments of Neurology (Drs. Krauss, Lesser, and Niedermeyer, and A. Abdallah) and Biostatistics (Dr. Thompson), School of Public Health, Johns Hopkins University, Baltimore, MD. Received December 3, 2004. Accepted in final form March 3, 2005. Address correspondence and reprint requests to Dr. Gregory Krauss, Meyer 2-147, 600 N. Wolfe St., Baltimore, MD 21287; e-mail: gkrauss@jhmi.edu. Copyright © 2005 by AAN Enterprises, Inc. 1879
  • 3. zures: mean 19.8 years (13.6, 25.9), p Ͻ 0.0001 (table 1). The clinical episodes for the patients with wicket rhythms were much longer in duration (mean 155.8 minutes) com- pared to patients with complex partial seizures (mean 2.4 minutes; log duration, p Ͻ 0.01). The average frequency of patients’ clinical episodes was similar for patients with wickets (mean 21 per year [0.43, 42.6]) and patients with complex partial seizures (mean 23.7 seizures per year [2.1, 45.2]; p ϭ 0.9). The duration of wicket rhythm bursts were longer (mean 0.66 seconds [0.5, 0.8]) compared to interictal epileptogenic patterns (mean 0.11 seconds [0.09, 0.12]; p Ͻ 0.001). EEG frequencies were similar between wicket and interictal epileptogenic patterns, with a slightly slower fre- quency for wicket rhythms (9.3 Hz [8.35, 10.21]) compared to interictal epileptogenic patterns (10.8 Hz [9.7, 12]; p ϭ 0.05). There was considerable heterogeneity in clinical symp- toms across patients in both groups (table 2). Signs and symptoms that differed between patients with wicket pat- terns and patients with seizures were as follows: sensory symptoms (mostly limb paresthesias) were uncommon in patients with epilepsy, while patients with partial-onset seizures were much more likely to have confusion and oral automatisms. Fainting symptoms occurred only in patients with wicket patterns. Both groups frequently reported con- fusion and histories of head trauma. Patients who experi- enced confusion, however, were 10 to 40 times more likely to have epilepsy after controlling for other covariates. This result is significant in models that control for age at symp- tom onset and EEG frequency or EEG frequency alone, and approaches significance when controlling for age at onset alone. The majority (52%) of patients with epilepsy had abnormal MRI (most commonly hippocampal atrophy, low grade tumor, encephalomalacia) compared to 16% of patients with wicket rhythms (nonspecific white matter changes, one subarachnoid cyst). An increase in the age at onset resulted in a decreased likelihood of having epilepsy, with a predicted OR of ap- Table 1 Clinical and EEG characteristics for patients with wicket patterns and epilepsy Wicket patients Epilepsy patients p Value Female, % 84.0 72.0 Head trauma, % 28.0 24.0 Log (episode duration), min 2.36 (1.22, 3.50) 0.50 (0.18, 0.83) 0.0013* Episode frequency/y 21.50 (0.43, 42.57) 23.65 (2.13, 45.17) 0.8835 EEG duration, s 0.66 (0.52, 0.81) 0.11 (0.09, 0.12) Ͻ0.0001 EEG frequency, Hz 9.28 (8.35, 10.21) 10.84 (9.70, 11.98) 0.0486 MRI, % Abnormal 16.0 52.0 0.025† Normal 60.0 36.0 No MRI 24.0 12.0 Values are % or mean (95% CI). p Values from the t test. * The natural log was included, since episode duration was highly skewed. † p Value from Fisher exact test. Table 2 Symptoms and signs for patients with wicket activity and epilepsy Variable Wicket patients, n ϭ 25 Epilepsy patients, n ϭ 25 p Value* Motor activity 0.0 20.0 0.050 Confusion 56.0 96.0 0.001* Psychic 20.0 4.0 0.189 Sensory 56.0 4.0 Ͻ0.001* Oral automatisms 0.0 40.0 0.001* Nausea 16.0 0.0 0.110 Staring 4.0 24.0 0.098 Fainting 32.0 0.0 0.004* Shaking 20.0 0.0 0.050 Weakness 20.0 0.0 0.050 Speech arrest 0.0 12.0 0.235 Vomiting 8.0 0.0 0.490 Aura prior 12.0 40.0 0.051 Other Rapid breathing, decreased ability to concentrate, burning sensation, headache Collapse, activity arrest, olfactory aura, wandering Group differences are evaluated by Fisher exact test. Values are %. * Significant with Bonferroni correction for multiple measures. 1880 NEUROLOGY 64 June (1 of 2) 2005
  • 4. proximately 0.9 for every year increase in the age at onset (figure 1). This is significant (p ϭ 0.001) after controlling for confusion and EEG frequency. Patients often had single discharges or brief bursts of wicket activity that appeared morphologically similar to interictal spikes and sharp waves (figure 2, A and B). All patients with wicket activity, however, also had long focal runs of semirhythmic 6- to 11-Hz activity that contained wickets and distinguished their EEG from interictal spikes and sharp waves and ictal EEG patterns (figure 3, A and B). EEG waveform durations greater than 0.26 seconds indicated a wicket pattern with a corresponding 100% sen- sitivity and specificity for this clinical group. Discussion. Epilepsy was incorrectly diagnosed in a group of patients with clinical episodes that were atypical for seizures; the misinterpretation of EEG wicket patterns contributed to patients’ misdiagno- sis. While this is a retrospective study, the case- control findings provide clinical clues that may help clinicians distinguish patients with nonepileptic epi- sodes and wicket patterns from patients with epilepsy. EEG wicket patterns are usually benign and do not suggest the presence of epilepsy.5 Within a single EEG recording, wickets may range in appearance from single sporadic spikes to trains of arciform dis- charges.6 Trains of wicket activity typically have a crescendo-decrescendo envelope and can often be found bilaterally over temporal regions, though not necessarily on both sides at the same time. Single wicket spikes are those that are commonly misinter- preted as temporal spikes or sharp waves due to their similarity in appearance.6 Interictal spikes and sharp waves often have a following slow wave that distinguishes them from isolated wickets. In our se- ries, patients with brief wicket patterns that might be mistaken for interictal spikes and sharp waves also had long runs of 6- to 11-Hz semirhythmic activ- ity over the same temporal regions. Interictal spikes and sharp waves were all brief in duration for our patient sample (Ͻ0.26 seconds), a factor that distin- guished patients with partial seizures from those with wickets. Occasionally, patients with partial sei- zures may have longer duration bursts of focal epi- leptogenic activity (spikes, sharp waves, and paroxysmal slowing). Wicket patterns are most common in people over age 33 years7 ; this is in accordance with the mid- adult age at onset of episodes seen in the nonepilep- tic group in this study. It has been reported that wicket activity may be associated with cerebrovascu- lar disease in some patients,8 however, this associa- tion has not been confirmed in controlled studies and is most commonly reported in patients with EEG wickets and focal slowing (“minor sharp and slow pattern”).3,9,10 Wicket activity has been classified as a normal variant EEG pattern. This term is meant to Figure 1. Distribution of age at onset of clinical episodes (n ϭ 25 for each group). Figure 2. (A) Wicket activity in a patient with episodic dizzi- ness. There is rhythmic 6-Hz activity, which occurs in brief bursts and longer trains. This wicket activity is maximal over the left temporal area, but was also present on the right. The patient has a history of a right cerebrovascular accident. (B) Right temporal sharp wave in a patient with complex partial seizures and MRI evidence of right mesial temporal sclerosis. Unlike the wicket activity, the sharp wave occurs in isolation without a buildup of arciform waveforms. June (1 of 2) 2005 NEUROLOGY 64 1881
  • 5. help de-emphasize an association between wicket ac- tivity and epilepsy. Following evaluation at our epilepsy clinic, study patients initially diagnosed with epilepsy were found to have alternative diagnoses, most commonly near- syncope, psychogenic nonepileptic seizures, anxiety, hyperventilation, migraine, or postconcussive syn- dromes. Many patients had typical symptoms of syn- cope or near-syncope: postural light-headedness or unconsciousness, slumping or falling, occasional stiffening or jerking but no full convulsions, pale- ness, and nausea.11,12 Many patients also had nonepi- leptic psychogenic seizures with features atypical for seizures, such as retained alertness despite bilateral motor signs and repeated sensory episodes lasting more than 4 minutes.13 These symptoms should sug- gest the possibility of diagnoses other than epilepsy when they occur. A limitation of this study is the retrospective de- sign and the limited sample size. During rereading of previous EEGs, records may have been classified as showing wicket activity rather than sharp waves or spikes based on patients’ atypical clinical presenta- tions. Wicket activity and epileptogenic activity, however, were confirmed on readings of additional EEG, with the electroencephalographer blinded to the clinical history and previous EEG findings. Moreover, 46% of patients with wicket activity also had spikes and sharp waves on their previous and Johns Hopkins University EEGs. These patients were confirmed to have epilepsy. Finally, the referral population from which the patients for this study were chosen is a limitation. Neurologists often noted in their consultations that they were uncertain of the etiology of patients’ clinical episodes due to their atypical features; nev- ertheless, they subsequently relied on incorrect EEG interpretations in making a diagnosis of epilepsy. Nonepileptic conditions are frequently misdiagnosed as epilepsy and this error can lead to many prob- lems, such as frustration for the patient when the misdiagnosis is realized, a delay in appropriate diag- nosis and treatment, and inappropriate treatment with antiepileptic drugs.11,14 Several patients were unnecessarily exposed to antiepileptic drugs for 2 or more years. Antiepileptic drugs are costly and pa- tients without epilepsy need not tolerate the side effects of such drugs, which are unlikely to control their episodes.15 Although the EEG is a useful diagnostic test for epilepsy, incorrect interpretations may lead to incor- rect diagnoses. While spikes and sharp waves are relatively specific for epilepsy, they are sometimes difficult to identify correctly: some patterns, includ- ing wickets, appear similar in appearance to interic- tal epileptogenic activity. Physicians should be cautious in diagnosing epilepsy in the presence of atypical clinical episodes combined with uncertain EEG findings.16 A useful clinical technique for deter- mining whether brief arciform transients are actu- ally fragments of a wicket rhythm is to see whether similar but prolonged wicket rhythms are present elsewhere in the EEG (see figure 3, A and B). Some patients may benefit from additional EEG recording to see whether brief transients are components of a wicket rhythm or, conversely, to see if true spikes and sharp waves might appear. A better understand- ing of normal variant patterns such as wickets is crucial to the prevention of epilepsy misdiagnosis.8 Figure 3. There is a brief burst of wicket activity in the left and right temporal leads (A). Six seconds later, there is more prolonged wicket activity (B), which is recorded maximally over the left temporal lobe. The more prolonged wicket activity helps distinguish the brief bursts of wicket activity from interictal spikes and sharp waves. 1882 NEUROLOGY 64 June (1 of 2) 2005
  • 6. References 1. Benbadis SR, Tatum WO. Overinterpretation of EEGs and misdiagnosis of epilepsy. J Clin Neurophysiol 2003;20:42–44. 2. Westmoreland BF. Epileptiform electroencephalographic patterns. Mayo Clin Proc 1996;71:501–511. Review. 3. Asokan G, Pareja J, Niedermeyer E. Temporal minor slow and sharp EEG activity and cerebrovascular disorder. Clin Electroencephalogr 1987;18:201–210. 4. StataCorp 2001. Stata Statistical Software. Release 7.0. Vol 1. College Station, TX: Stata Corporation, 2001;209. 5. Klass DW, Westmoreland BF. Nonepileptogenic epileptiform electroen- cephalographic activity. Ann Neurol 1985;18:627–635. 6. Reiher J, Lebel M. Wicket spikes: clinical correlates of a previously undescribed EEG pattern. Can J Neurol Sci 1977;4:39–47. 7. Batista MS, Coelho CF, de Lima MM, Silva DF. A case-control study of a benign electroencephalographic variant pattern. Arq Neuropsiquiatr 1999;57:561. 8. Kellaway P. Orderly approach to visual analysis: elements of the nor- mal EEG and their characteristics in children and adults. In: Ebersole JS, Pedley TA, eds. Current practice of clinical electroencephalography, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 2003;127–132. 9. Bruens JH, Gastaut H, Giove G. Electroencephalographic study of the signs of chronic vascular insufficiency of the Sylvian region in aged people. Electroencephalogr Clin Neurophysiol 1960;12:283–295. 10. Koshino Y, et al. Temporal minor slow and sharp activity in psychiatric patients. Clin Electroencephalogr 1990;21:225–232. 11. Smith D, et al. The misdiagnosis of epilepsy and the management of refractory epilepsy in a specialist clinic. QJM 1999;92:15–23. 12. Bergfeldt L. Differential diagnosis of cardiogenic syncope and seizure disorders. Heart 2003;89:353–358. 13. Fleisher W, et al. Comparative study of trauma-related phenomena in subjects with pseudoseizures and subjects with epilepsy. Am J Psychia- try 2002;159:660–663. 14. Scheepers B, Clough P, Pickles C. The misdiagnosis of epilepsy: find- ings of a population study. Seizure 1998;7:403–406. 15. Chadwick D, Smith D. The misdiagnosis of epilepsy. BMJ 2002;324: 495–496. 16. Worrell GA, Lagerlund TD, Buchhalter JR. Role and limitations of routine and ambulatory scalp electroencephalography in diagnosing and managing seizures. Mayo Clin Proc 2002;77:991–998. Review. ACTIVATE YOUR ONLINE SUBSCRIPTION At www.neurology.org, subscribers can now access the full text of the current issue of Neurology and back issues to 1999. Select the “Login instructions” link that is provided on the Help screen. Here you will be guided through a step-by-step ac- tivation process. Neurology online offers: • Access to journal content in both Adobe Acrobat PDF or HTML formats • Links to PubMed • Extensive search capabilities • Complete online Information for Authors • Examinations on designated articles for CME credit • Access to in-depth supplementary scientific data June (1 of 2) 2005 NEUROLOGY 64 1883
  • 7. DOI 10.1212/01.WNL.0000163991.97456.03 2005;64;1879-1883Neurology G. L. Krauss, A. Abdallah, R. Lesser, et al. with epilepsy Clinical and EEG features of patients with EEG wicket rhythms misdiagnosed This information is current as of June 13, 2005 Services Updated Information & http://www.neurology.org/content/64/11/1879.full.html including high resolution figures, can be found at: References 1 http://www.neurology.org/content/64/11/1879.full.html##ref-list- at: This article cites 14 articles, 3 of which you can access for free Citations icles http://www.neurology.org/content/64/11/1879.full.html##otherart This article has been cited by 8 HighWire-hosted articles: Subspecialty Collections http://www.neurology.org//cgi/collection/eeg_ EEG http://www.neurology.org//cgi/collection/all_epilepsy_seizures All Epilepsy/Seizures following collection(s): This article, along with others on similar topics, appears in the Permissions & Licensing http://www.neurology.org/misc/about.xhtml#permissions or in its entirety can be found online at: Information about reproducing this article in parts (figures,tables) Reprints http://www.neurology.org/misc/addir.xhtml#reprintsus Information about ordering reprints can be found online: