The breach rhythm - PDF Archive

Invited Review
The breach rhythm
Francesco Brigo ⇑ , Rosario Cicero, Antonio Fiaschi, Luigi Giuseppe Bongiovanni
Department of Neurological, Neuropsychological, Morphological and Movement Sciences, Section of Clinical Neurology, University of Verona, Italy
article info
Article history:
Accepted 7 July 2011
Available online 26 August 2011
Keywords:
Brain surgery
Breach rhythm
EEG
Epileptiform abnormalities
Contents
highlights
EEG after craniotomy are difficult to interpret because of breach rhythm.
Breach rhythm can mimic epileptiform abnormalities and lead to misinterpretations.
Breach rhythm appears to have a little relationship to epilepsy.
In an EEG with breach rhythm, it is very important to adopt a ‘conservative’ reading.
abstract
Electroencephalography (EEG) recordings obtained after craniotomy are difficult to interpret because of
the presence of a breach rhythm (BR) consisting of unfiltered high-voltage physiological waveforms,
sometimes with a spiky and irregular morphology, that can mimic interictal epileptiform abnormalities
and may therefore lead to misinterpretations. In this article, we review EEG features of BR and give some
technical tips to properly interpret BR and to make a correct differential diagnosis with epileptiform
abnormalities. As BR itself has no relationship to epilepsy, it is very important to adopt a ‘‘conservative’’
reading, having a high threshold to call epileptiform abnormalities.
Ó 2011 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights
reserved.
1. Introduction ........................................................................................................ 2116
2. EEG features ........................................................................................................ 2117
3. Genesis . . . . ........................................................................................................ 2117
4. Systematic review of the literature. . . . . . . . . . . . . . . . . ..................................................................... 2117
5. Epileptiform abnormalities and BR: problems in interpretation and technical tips. . . . . . . . . . . . . . . . . ............................... 2118
6. Conclusions. ........................................................................................................ 2119
Disclosure/Conflict of interest. . ........................................................................................ 2120
References . ........................................................................................................ 2120
1. Introduction
Breach rhythm (BR), or, more properly, breach effect (Stern and
Engel, 2005), is defined as a focal increase in the amplitude activity
of alpha, beta and mu rhythms which tends to develop over or near
the area of a bony skull defect, such as after craniotomy or cranial
surgery (Cobb et al., 1979). By itself, it is not indicative of brain
⇑ Corresponding author. Address: Department of Neurological, Neuropsychological,
Morphological and Movement Sciences, Section of Clinical Neurology, University
of Verona, Piazzale L.A. Scuro, 10-37134 Verona, Italy. Tel.: +39 0458124174;
fax: +39 0458124873.
E-mail address: dr.francescobrigo@gmail.com (F. Brigo).
Clinical Neurophysiology 122 (2011) 2116–2120
Contents lists available at ScienceDirect
Clinical Neurophysiology
journal homepage: www.elsevier.com/locate/clinph
dysfunction and may be considered as an expected physiologic
consequence of a skull defect (Cobb et al., 1979; Stern and Engel,
2005), unless associated with spikes or focal slowing. Differentiating
between BR and epileptiform abnormalities occurring in the
same area may be challenging, since sharpening and irregular
morphology of BR may lead to misinterpretations.
As a matter of fact, its sharply contoured morphology may be
considered as an epileptiform abnormality, thus leading to a
misdiagnosis of epilepsy and to an unnecessary treatment with
antiepileptic drugs. On the other hand, epileptiform abnormalities
arising from the same area of BR may be overlooked and go undiagnosed.
Therefore, performing a correct differential diagnosis is of
paramount importance, given its relevant clinical consequences.
1388-2457/$36.00 Ó 2011 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.clinph.2011.07.024

In this article, we review EEG features of BR and give some technical
tips to properly interpret BR and to make a correct differential
diagnosis with epileptiform abnormalities.
2. EEG features
BR consists of a focal, asymmetrical, high-voltage 6–11 Hz
activity, sometimes admixed with lower or faster components
(Fig. 1). It has often larger arch-like shaped waveforms, and sometimes
a spiky morphology. Frequently, beta and alpha, mu or theta
activity is admixed, and BR can manifest as an irregular rhythm
sometimes associated with sharp activity. Very often it consists
of a high-amplitude rhythmic spiky or sharply contoured activity
(Niedermeyer, 2005; Blume et al., 2011). Polymorphic delta activity
associated with BR should raise a suspicion of brain damage
(Stern and Engel, 2005). BR may be easily blocked by physical
movement such as contralateral movement, if located over central
region (because of the coexistence of an underlying normal mu
rhythm); if over the temporal, it is not. BR occurs in wakefulness,
but sometimes may persist also in sleep, thus permitting a differentiation
with electromyographic artefacts which may coexist
with BR, but disappear in sleep (Stern and Engel, 2005); in II stage
of sleep it can manifest as a voltage increase in spindles.
3. Genesis
The mechanisms underlying the genesis of BR are largely unknown.
Bone acts as a filter attenuating higher frequencies. Increased
amplitude and faster frequencies of BR might therefore
reflect enhancement of the underlying cerebral rhythms, such as
the mu rhythm, due to a reduced filtering effect (less filtering of
high frequencies or reduced electrical impedance) on the EEG signal
caused by the bone defect (Cobb et al., 1979; van Doorn and
F. Brigo et al. / Clinical Neurophysiology 122 (2011) 2116–2120 2117
Fig. 1. EEG showing BR involving mainly right fronto-central regions. Sensitivity 7 uV/mm; TC 0.3 s; HF: 50.0 Hz; 20 s/page.
Cherian, 2008). Bone is the major resistive element between the
cortex and scalp electrode, with approximate resistance for 1 cm 2
of skull estimated as 40,000 X, compared with 12,000 X of dura
mater and 1000 X of scalp (Rémond 1977; Cobb et al., 1979). Absence
of bone therefore results in a significant increase in current
from cortex to scalp, so that BR represents unfiltered brain activity
through a skull defect (Cobb et al., 1979; Niedermeyer, 2005).
Interestingly, when there is a breach of the frontal bone, the eyemovement
artefact has lower voltage ipsilateral to the skull defect;
it is thought to occur by virtue of a shunting of the eye potential
through the skull (Fisch, 1999).
4. Systematic review of the literature
Although most atlases and textbooks of EEG interpretation
discuss this topic, in the literature there are very few studies specifically
dealing with BR, despite the presence of several works
concerning true epileptiform abnormalities after epilepsy surgery.
A MEDLINE search conducted using ‘‘breach rhythm’’ OR ‘‘breach
activity’’ (free term) and ‘‘Electroencephalography’’ (MeSH term)
yielded only seven results. A manual search of the references
quoted in the identified works yielded four additional works dealing
with BR (Fischgold et al., 1952; Kendel, 1970; Courjon and
Scherzer, 1972; Rémond, 1977).
Berger’s first EEGs were all recorded over bone defects, as well
as EEGs obtained by Adrian and Matthews, the results of recording
from patients with skull holes. Fischgold et al. (1952) coined the
term ‘‘breach’’ (brèche), to indicate traumatic bone defects,
distinguishing between brèches traumatiques and volets (flaps)
neurochirurgicaux. Fischgold initially described effects of bone
defects on the EEG, noting an enhanced, sharp activity, which
was probably related to the mu rhythm described in the same year
by Gastaut et al. (1952). Both Fischgold (Fischgold et al., 1952) and

2118 F. Brigo et al. / Clinical Neurophysiology 122 (2011) 2116–2120
Gastaut (Gastaut et al., 1952), although accepting a significant role
of bone and dura-mater absence, considered this enhanced activity
as secondary to meningo-cortical adhesions with admixed gliosis,
without providing evidence of such a statement.
Kendel (1970) reported 30 patients with skull defects, comparing
EEG amplitudes over the defect and the homologous contralateral
area, finding an increase over the skull defect of up to 5 times,
with a mean ratio of 150%. Such an increase of amplitude was
attributed to lowered resistance by Courjon and Scherzer (1972).
In 1979 Cobb (Cobb et al., 1979), who was the first to use the
term ‘breach rhythm’, reported EEG features of 33 patients with
skull defects, describing 21 cases with skull defects involving or
near to central (C3/C4) and midtemporal (T3/T4) electrodes, in
whom EEG showed sharply focal mu-like rhythms at 6–11 c/s, usually
associated with faster components. Although the former was
responsive to fist clenching (but not to eye opening), the latter
was unresponsive to any stimulus. In both cases, waves often
had spike-like negative components, sometimes admixed with true
spikes and slow waves with the same restricted focus and responsiveness.
Bone replacement could lead to some reduction of the
midtemporal rhythm. Cobb concluded that the term ‘breach
rhythm’ was preferable to ‘mu’ or ‘mu-like’ rhythm because of such
a complexity in EEG features, and stated that BR, even when very
sharp in morphology, appears to have little relationship to epilepsy
and is not an indicator of recurrence of a tumour.
Other than surgical, developmental or traumatic skull defect, BR
was later described with osteolytic bone metastasis of the skull
(Radhakrishnan et al., 1994) or with multiple myeloma skull lesion
(van Doorn and Cherian, 2008).
BR was also investigated (Niedermeyer 1990; Niedermeyer
1991) because of the possibility of recording a third type of
rhythmical activity in alpha- (or sub-alpha-) frequency (apart
from posterior dominant alpha rhythm and rolandic mu rhythm)
over the temporal lobe and especially over the midtemporal region.
This rhythm, which is undetectable in scalp EEG, becomes
quite prominent and dominates the activity of the temporal lobe
with the use of epidural electrodes. Its reactiveness, as well as its
neurophysiologic and psychophysiologic significance, are still unclear.
Subsequent observations in patients with cerebrovascular
disorder and in subjects with congenital bone thinning or with
skull defect after intracranial surgery supported the existence of
intrinsic alpha-like activity of the temporal lobe, independent of
posterior dominant alpha rhythm of the occipital lobe (Shinomiya
et al., 1999).
A recent study conducted in 20 patients after craniotomy has
compared EEG and magnetoencephalography (MEG) in evaluating
BR and interictal epileptiform discharges (Lee et al., 2010). Larger
inter-rater variability was found for EEG as compared with MEG.
Sharp waveforms that were difficult to evaluate on EEG were found
to be more easily interpretable on MEG. Authors concluded that
MEG is less affected by the BR and should be therefore considered
as an adjunctive study in patients with BR for evaluation of interictal
epileptiform discharges and cerebral dysfunction.
5. Epileptiform abnormalities and BR: problems in
interpretation and technical tips
BR occurs only over skull defects, so that it may be very limited
in space. A bipolar montage may therefore be appropriate to identify
BR, given its higher spatial resolution. EEG technician should
always ask the patient about previous head injury or brain surgery,
in order to evaluate whether BR is likely to be present. Palpation of
the scalp alone may not be sufficient because the skull may have
been replaced by bone (or acrylic) material which may not eliminate
the BR (Cobb et al., 1979; Stern and Engel, 2005).
Sharpening and irregular morphology of BR may be erroneously
considered as an epileptiform abnormality. Especially when mu
and beta rhythms are present, waveforms which are actually
abnormally high amplitude physiologic rhythms may resemble
sharp waves or spikes.
‘Conservative’ reading should be strongly emphasized during
EEG training, since all epileptologists agree that overreading is
much more harmful than underreading (Benbadis, 2007). Especially
when a BR is present, it is very important to have a high
threshold to call epileptiform abnormalities.
Conversely, it is very important, although sometimes quite difficult,
not to overlook a sharp wave or spike arising from the same
region of BR region.
Following EEG aspects may help neurologist and the EEG technician
to properly interpret BR and to make a correct differential
diagnosis with true epileptiform abnormalities.
(1) In pure BR there are no after-going slow waves. However,
when BR is associated with polymorphic delta activity, one
must carefully distinguish between a true after-following
slow wave and a random combination of a sharp BR and
delta waveforms (Fig. 2).
(2) In pure BR there is no spread of ‘‘suspicious activity’’ to other
areas (Fig. 2).
(3) Sleep recordings may be useful to differentiate BR from epileptiform
abnormalities. If constituted mainly by enhanced
underlying rhythms present in the awake state and disappearing
in drowsiness and sleep (such as mu and posterior
dominant alpha rhythms), BR may attenuate in amplitude
or disappear (van Doorn and Cherian, 2008). If admixed with
‘third midtemporal alpha-like rhythm’, BR may linger into
drowsiness and even into light non-rapid eye movement
(NREM) sleep (Niedermeyer, 1990). Conversely, sleep has
great impact on activation of interictal epileptiform abnormalities
(Malow et al. 2000; Parrino et al. 2001), which are
in general facilitated during NREM sleep and relatively
inhibited during REM sleep (their density increases with
descending sleep depth) (Minecan et al., 2002).
(4) Since mu rhythm within BR may be misinterpreted as a
pathologic epileptiform activity, it is important to test for
reactivity of the mu rhythm (e.g., the attenuation when the
patient is asked to move a contralateral limb). The reactivity
of BR, when present, is therefore indicative of a normal pattern,
such as that of an enhanced underlying mu rhythm;
however, the lack of reactivity does not rule out the presence
of a normal pattern (such as ‘‘third rhythm’’ of temporal
lobe).
(5) Comparing to BR, true epileptiform abnormalities have different
frequency and amplitude (Fig. 2).
(6) The presence of a BR admixed with physiological posterior
dominant alpha rhythm may resemble sharp waves, especially
on temporo-occipital derivations in bipolar montage.
In such case, the sharply contoured morphology can be
attenuated by eye opening.
(7) It is important to keep in mind that when a skull defect is
present over the temporal regions, benign epileptiform patterns,
such as wicket spikes can appear more prominent
(Mushtaq and Van Cott, 2005).
(8) EEG filters should be used carefully: reducing too much high
frequency filters’ values to attenuate the BR, may filter out
the higher frequencies of BR, so that what is left could actually
resemble spikes/sharp-waves. The same problem may
occur when muscle artifacts are admixed with BR. Electromyographic
artefacts may be easily distinguished by BR
because of their much higher frequency components, provided
that an appropriate high-frequency filter value has

een chosen: filtering out the muscle activity only attenuates
these signals, and may lead to an erroneous misdiagnosis
of true epileptiform abnormalities within BR.
(9) In case of excessively high amplitude, reducing sensitivity
may be useful to better analyse EEG features of BR, so that
sometimes epileptiform abnormalities may be more easily
legible (Fig. 2).
(10) From a technical point of view, one common cause of overreading
a BR is to give an excessive emphasis on ‘phase
reversals’ which sometimes may be seen in BR. Phase reversals
are not always indicative of abnormalities, as, according
to basic principles of polarity and localization, they only
indicate location (maximum voltage) (Benbadis, 2007):
bipolar montage phase reversals only localise a waveform
and have no significance for the diagnosis of epilepsy. The
F. Brigo et al. / Clinical Neurophysiology 122 (2011) 2116–2120 2119
Fig. 2. BR involving all left derivations in a patient who underwent hemicraniectomy shown at different sensitivities. This figure represents therefore an extreme example of
unusually widespread BR. The patient suffers from epileptic seizures and is currently treated with carbamazepine. (A) 14 uv/mm: Sharply contoured transients clearly emerge
from BR because of their higher amplitude, sharper morphology and different frequency. They also spread to contralateral regions. Polymorphic slow waves are admixed
within BR (suggestive of underlying brain pathology). (B) Sensitivity 50 uV/mm: at this sensitivity it is more evident that epileptiform abnormalities with after-going slow
waves are admixed with and stand out from BR. TC 0.3 s; HF: 70.0 Hz; 20 s/page.
presence of phase reversals in BR should therefore be evaluated
carefully and in a rather ‘conservative’ way, before diagnosing
the presence of epileptiform abnormalities.
(11) Progression of a lesion (e.g., tumour) beneath the skull
defect or burr hole should be suspected if serial EEG recordings
show attenuation of pre-existing high amplitude and/or
the presence of focal slow waves.
6. Conclusions
EEGs obtained after craniotomy are difficult to interpret because
of the presence of a BR consisting of unfiltered high-voltage
physiologic waveforms, sometimes with a spiky and irregular morphology
that can mimic interictal epileptiform abnormalities.
Some EEG aspects may help to distinguish between BR and

2120 F. Brigo et al. / Clinical Neurophysiology 122 (2011) 2116–2120
epileptiform discharges. Despite its sharp morphology, BR itself
has no relationship to epilepsy. In presence of BR it is therefore
advisable to adopt a ‘conservative’ reading, having a high threshold
to call epileptiform abnormalities in order to avoid a misdiagnosis
of epilepsy due to an over-interpretation of non-epileptic sharp
patterns, which may have serious clinical consequences: an ‘abnormal’
EEG is too often considered as an irrevocable sentence of epilepsy,
leading to an antiepileptic treatment which is not only
ineffective, but also expensive and sometimes harmful for the
patient.
Disclosure/Conflict of interest
None.
References
Benbadis SR. Errors in EEGs and the misdiagnosis of epilepsy: importance, causes,
consequences, and proposed remedies. Epilepsy Behav 2007;11(3):257–62.
Nov.
Blume WT, Holloway GM, Kaibara M, Young GB. Nonepileptiform abnormalities. In:
Blume WT, Holloway GM, Kaibara M, Young GB, editors. Atlas of Pediatric and
Adult Electroencephalography. Philadelphia: Lippincott Williams & Wilkins;
2011. p. 487.
Cobb WA, Cobb WA, Guiloff RJ, Cast J. Breach rhythm: the EEG related to skull
defects. Electroencephalogr Clin Neurophysiol 1979;47(3). Sep.
Courjon J, Scherzer E. Late effects of head injury. Handbook of
Electroencephalography and Clinical neurophysiology 1972;Vol
14B. Amsterdam: Elsevier; 1972. p. 47–82.
Fisch BJ. Fisch & Spehlmann’s EEG primer: basic principles of digital and analog EEG.
3rd printing, rev. and enl. Elsevier Health Sciences 1999:109–10.
Fischgold H, Pertuiset B, Arfel-Capdeveille G. Quelques particularités
électroencéphalographiques au niveau des brèches et des volets
neurochirurgicaux. Rev Neurol 1952;86:126–32.
Gastaut H, Terzian H, Gastaut Y. Etude d’une activité électroencéphalographique
méconnue: ‘le rhythme rolandique en arceau’. Marseille méd 1952;89:296–310.
Kendel K. EEG – Veränderungen bei Knochenlücken. Electromedica 1970;2:195–7.
Lee JW, Tanaka N, Shiraishi H, Milligan TA, Dworetzky BA, Khoshbin S. Evaluation of
postoperative sharp waveforms through EEG and magnetoencephalography. J
Clin Neurophysiol 2010;27(1):7–11. Feb.
Malow A, Bowes RJ, Ross D. Relationship of temporal lobe seizures to sleep and
arousal: a ombined scalp-intracranial electrode study. Sleep 2000;23(2):231–4.
Mar 15.
Minecan D, Natarajan A, Marzec M, Malow B. Relationship of epileptic seizures to
sleep stage and sleep depth. Sleep 2002;25(8):899–904. Dec.
Mushtaq R, Van Cott AC. Benign EEG Variants. Am J EEG Technol 2005;45:88–101.
Niedermeyer E. Alpha-like rhythmical activity of the temporal lobe. Clin
Electroencephalogr 1990;21(4):210–24. Oct.
Niedermeyer E. The ‘‘third rhythm’’: further observations. Clin Electroencephalogr
1991;22(2):83–96. Apr.
Niedermeyer E. The normal EEG of the waking adult. In: Niedermeyer E, Lopes da
Silva F, editors. Electroencephalography: basic principles, clinical applications,
and related fields. Baltimore (MD): Williams & Wilkins; 2005. p. 178.
Parrino L, Smerieri A, Terzano MG. Combined influence of cyclic arousability and
EEG synchrony on generalized interictal discharges within the sleep cycle.
Epilepsy Res 2001;44(1):7–18. Apr.
Radhakrishnan K, Silbert PL, Klass DW. Breach activity related to an osteolytic skull
metastasis. Am J EEG Technol 1994;34:1–5.
Rémond A. Origin and transformation of the electrical activities which result in the
electroencephalogram. Handbook of Electroencephalography and Clinical
neurophysiology 1977;Vol. 11A. Amsterdam: Elsevier; 1977. p. 21.
Shinomiya S, Fukunaga T, Nagata K. Clinical aspects of the ‘‘third rhythm’’ of the
temporal lobe. Clin Electroencephalogr 1999;30(4):136–42. Oct.
Stern JM, Engel Jr J. Breach effect. In: Stern JM, Engel Jr J, editors. Atlas of EEG
patterns. Philadelphia: Lippincott Williams & Wilkins; 2005. p. 101–3.
van Doorn J, Cherian PJ. Neurological picture. Breach rhythm related to a solitary
skull lesion caused by multiple myeloma. J Neurol Neurosurg Psychiatry
2008;79(7):819. Jul.