Breach Rhythm

Article Author:
Renu Kadian
Article Author:
Lalitha Padmanabha Vemireddy
Article Editor:
Anil Kumar
Updated:
9/18/2020 8:56:13 AM
PubMed Link:
Breach Rhythm

Introduction

The breach rhythm, also known as the breach effect, is a benign EEG pattern with an epileptiform morphology, caused by a skull abnormality. A focal skull defect, like after a craniotomy, can cause an increase in the amplitude of alpha, beta, and mu rhythms, leading to the breach effect. Breach rhythm and epileptiform activity in the same area can be challenging to differentiate. Breach rhythm typically has sharp contours and irregular morphology, usually have a frequency of 6 to 11 Hz but may be associated with faster or slower wave activity. It may sometimes be hard to differentiate from actual epileptiform activity in the same area, which can lead to under or overdiagnosis of epilepsy and thus can have significant clinical consequences.[1][2]

EEG Features of Breach Rhythm

An electroencephalogram (EEG) is a noninvasive test for providing neurophysiological activity of the brain. It is usually done by placing electrodes over the scalp which measures the activity of neurons.[3] It is very important to understand how to differentiate between normal/benign variants of EEG vs pathological variants of EEG. The benign variants of EEG are considered normal but can be confused with epileptiform activity. Accurate recognition of benign variants in the EEG is crucial to avoid an errant diagnosis of epilepsy.[4]

Breach rhythm typically is a focal, asymmetrical, high-voltage activity. It often has arch-like waveforms, sometimes having spiky morphology. It can manifest as an irregular rhythm sometimes associated with sharp activity. Breach rhythm is most prominent when recorded over central and temporal regions. Breach rhythm can be identified easily when it occurs in serial trains. Single, spike-like, or sharp-contoured waveforms are more likely to be mistaken for epileptiform activity. These waveforms should be compared with waveforms of the rhythmic activity constituting breach rhythm to determine if these are distinct waveforms or similar to those constituting the breach rhythm. The absence of after coming slow-wave components and lack of spread to other areas is characteristic of breach rhythm. Brain damage should be suspected if breach rhythm is associated with polymorphic delta activity. If the breach rhythm is located over the central region, it can be blocked by physical movement due to the presence of an underlying normal mu activity. Breach rhythm can sometimes persist during sleep. It can manifest as a voltage increase in spindles in stage 2 of sleep.[2]

Etiology

The breach effect occurs due to an increase in the amplitude of alpha, beta, and mu rhythm activity over or near an area of a bony defect on the skull, usually post-surgical craniotomy site. Skullbone normally acts as a filter for brain electrical activity and attenuates the higher frequencies. An increase in amplitude and frequency of the breach effect is due to the decrease in electrical impedance caused by reduced filtering from the skull defect. Small skull defects, for example, a burr hole, is unlikely to produce a breach effect, as the field detected by each electrode is larger than the hole.[1][2]  There were also reports of breach rhythm being related to the functional state of underlying brain tissue.[5] Lyudmilov et al noticed that after a seizure event in a patient with craniotomy, EEG revealed subclinical seizure patterns until these were suppressed by an antiseizure medication, then the breach rhythm was seen. So they mentioned that breach rhythm could be suppressed due to todd's paralysis/post-seizure subclinical activity [5].

In certain cases like astrocytoma, there has been a case that reported either attenuation or loss of the breach rhythm can be an initial sign of tumor progression.[6] There are also reports of breach rhythm being developed over a solitary skull lesion due to multiple myeloma.[7]

Epidemiology

Breach rhythm is a rare benign variant of EEG. The epidemiology of breach rhythm is not known.

Pathophysiology

Breach rhythm was described in 1979 by Cobb and associates. Breach rhythm refers to a change in the transmission of EEG waves through a skull defect. Bone offers major resistance between cortex and scalp electrodes. One cm2 of the skull provides about 40,000-ohms resistance, dura mater about 12,000 ohms, and scalp about 1000 ohm resistance. Therefore, there is a significant increase in electrical activity from cortex to scalp when bone between them is absent. These events are spiky, sharply-contoured waveforms. Breach rhythm is most prominent in the central and temporal regions. [1][2][8]

Breach rhythm is not due to the abnormality of the brain; it is due to a skull defect.

History and Physical

Obtaining a surgical history and history of brain trauma is important. Skull defects can be missed on palpation because an artificial material may have replaced a skull defect.[2]

Evaluation

It is vital to identify breach rhythm while interpreting EEG to avoid misinterpretation of epileptiform activity.

It is important to inquire about the patient's surgical history and any history of head trauma to evaluate if breach rhythm is likely to be present. The palpation of the scalp may not be sufficient. Breach rhythm is seen over skull defects and abruptly diminishes beyond the margin of the defect. It is best appreciated by bipolar montage, due to its higher spatial resolution.[2]

Pure breach rhythm does not have an after going slow wave. There is no spread of activity to other areas of the brain. Sleep recordings can aid differentiation between breach rhythm and epileptiform activity.[1][2]

In general, interictal epileptiform abnormalities are facilitated during NREM sleep and inhibited during REM sleep. If breach rhythm is constituted mostly by enhanced underlying rhythms, breach rhythm will attenuate or disappear during drowsiness and sleep. It may linger into drowsiness and light NREM sleep if breach rhythm is mixed with a mid-temporal, alpha-like rhythm. Mu rhythm within breach rhythm can be tested for reactivity by asking the patient to move the contralateral limb. Attenuation on doing so suggests reactivity of breach rhythm and is indicative of a normal pattern; however, lack of reactivity does not rule out the presence of normal rhythm.[2][1]

EEG filters should be used carefully. Filters to reduce too-high frequency may filter out the higher frequencies of breach rhythm, but the left out activity could resemble spikes or sharp waves. Muscle artifacts usually can be easily identified by their much higher frequency component, provided an appropriate high-frequency filter be chosen. Filtering out muscle activity will attenuate the signals and may be confused for epileptiform abnormalities within the breach rhythm.[1][8][2]

Treatment / Management

Breach rhythm is a benign variant and does not warrant treatment. Attenuation of pre-existing high amplitude and/or presence of focal slow waves on serial EEG recordings may suggest the progression of the lesion beneath the skull defect.

A "conservative" reading is encouraged by most specialists since most believe that over-reading is likely more harmful than under-reading.[2] When in doubt, brain imaging like CT head and MRI head can be used to determine if any focal lesion is causing seizure activity.

Differential Diagnosis

Interictal epileptiform discharges include:

  • Paroxysmal fast activity
  • Beta frequency activity
  • Electromyographic artifact

It is important to differentiate the breach rhythm from interictal epileptiform discharges by scrutinizing the surrounding background activity. Polyphasic interictal discharges are complex with a slow wave and have a characteristic morphology that does not resemble the background activity. Breach rhythm can be differentiated from beta activity by their distribution. Normal beta activity is bilateral but may vary in distribution. The breach effect has a clearly circumscribed region of increased amplitude. The paroxysmal fast activity appears in bursts with an intervening return to asymmetric baseline. EMG artifacts occur in regions with overlying muscle, most commonly frontal and temporal regions. EMG artifacts can be differentiated by their inconsistent presence and much higher components.[8][2]

Prognosis

As breach rhythm is a benign variant, the prognosis is favorable.

Enhancing Healthcare Team Outcomes

Breach rhythm is due to bone abnormality and not due to brain pathology. Breach rhythm can be mistaken for epileptiform activity. An important distinction between the breach rhythm and epileptiform abnormality is the absence of after coming slow-wave and lack of spread to other areas of the brain. Breach rhythm occurs over the area of the skull defect and abruptly disappears at the margin of the skull defect. EEG technicians should always ask the patient about any history of brain surgery or head injury before performing the EEG.[1][2][8]


References

[1] Cobb WA,Guiloff RJ,Cast J, Breach rhythm: the EEG related to skull defects. Electroencephalography and clinical neurophysiology. 1979 Sep     [PubMed PMID: 90597]
[2] Brigo F,Cicero R,Fiaschi A,Bongiovanni LG, The breach rhythm. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2011 Nov     [PubMed PMID: 21872525]
[3] Light GA,Williams LE,Minow F,Sprock J,Rissling A,Sharp R,Swerdlow NR,Braff DL, Electroencephalography (EEG) and event-related potentials (ERPs) with human participants. Current protocols in neuroscience. 2010 Jul     [PubMed PMID: 20578033]
[4] Mari-Acevedo J,Yelvington K,Tatum WO, Normal EEG variants. Handbook of clinical neurology. 2019     [PubMed PMID: 31277844]
[5] Lyudmilov C,Petersone D,Schmidt C,Bösel J,Rösche J, Breach Rhythm May Be Suppressed as a Form of Todd's Paralysis. Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society. 2020 May     [PubMed PMID: 31977570]
[6]     [PubMed PMID: 23820313]
[7]     [PubMed PMID: 21687305]
[8] Westmoreland BF,Klass DW, Unusual EEG patterns. Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society. 1990 Apr     [PubMed PMID: 2187021]