Author: Poothrikovil, Rajesh P
Date published: March 1, 2012
Subclinical rhythmic electrographic discharge of adults (SREDA) first described in 1981 as a distinctive rhythmic EEG pattern in a series of 65 adult patients (Westmoreland and Klass 1981) is considered a benign epileptiform variant usually seen in older people in wakefulness. It is of little diagnostic significance and has a low incidence rate of 0.04%. The pattern consists of sharp contoured 5 to 7 Hz theta activity with an amplitude ranging from 40 to 100 µ V. SREDA usually has a widespread, bilaterally synchronous distribution typically maximal over parietal and posterior temporal area lasting for few seconds to several minutes. This pattern usually begins abruptly or with an interrupted onset consisting of high amplitude discharges which subsequently continue as a stable, non-evolving, and sinusoidal theta. The pattern may be aborted abruptly or gradually merge with the background. SREDA is mostly seen in wakefulness particularly during hyperventilation without altering patient's level of consciousness. It may occur more than once during a single EEG recording with varying intervals and may remain unchanged with eyes open. Unusual variants of SREDA were reported in 1997 with atypical features such as predominant delta frequency, anterior and focal distribution, bifid morphology, presence in sleep, and prolonged duration (Westmoreland and Klass 1997). It is important to successfully identify SREDA to avoid misdiagnosis. We report SREDA in a patient with primary generalized epilepsy which shows some atypical features and mimics a secondarily generalized partial seizure.
A routine EEG was performed on a 44-year-old female who has a history of epilepsy. Her seizures started when she was 16 years old and were characterized by morning myoclonus and frequent generalized tonic clonic seizures. Her seizures were fairly well controlled with sodium valproate and the frequency decreased to one to two per month. These symptoms were suggestive of juvenile myoclonic epilepsy (JME). With dose adjustment, she was seizure free for more than two years. Unfortunately due to poor compliance her seizures recurred with infrequent morning myoclonus. She was referred for an electroencephalographic assessment. Her last seizure was a few weeks before the EEG.
Digital EEG was performed with a Comet® series system (Grass Technologies, An Astro-Med, Inc. Subsidiary, West Warwick, Rhode Island, USA) with HFF at 70 Hz and LFF at 0.3 Hz. Notch filter was off during the EEG recording. Electrodes were applied according to the International 10-20 System of electrode placement and impedances were kept at or below 5,000 Ohms. The patient was fully co-operative and communicated well during the electrode hook-up and recording. The background activity consisted of 13 to 15 Hz beta activity of low amplitude (about 20 µ?) which was reactive to eye opening and closure. During hyperventilation (at about 70 seconds) a fairly abrupt, paroxysmal build-up of sharp contoured 7 to 8 Hz theta activity was noted over the right parietal area with spread to the posterior temporal (Figures 1, 2, 3, and 4). Minor evolution in amplitude noted after a few seconds reached a maximum voltage of 75 µ V. Subsequent spread to the left parieto-temporal area was seen seven seconds following the onset of the pattern over right parietal. In the bipolar montage, the sharply contoured waves had phase reversals in P4 and T6 over the right hemisphere and in P3 and T5 over the left hemisphere. In the referential montage (ipsilateral ear reference) amplitude was obviously higher at P4 and at P3/C3. This pattern lasted for about 25 seconds, during which patient did not show any behavioral alterations. She continued hyperventilating and answered all queries and was able to perform arithmetic during this period. She was puzzled and a bit disturbed for being questioned like this. The pattern suddenly subsided while checking the patient's response.
Several similar electrographic episodes were noted lasting variable durations. One of these episodes lasted for nearly 40 seconds with waxing and waning of rhythmic activity. Presence of this electrographic phenomenon was observed with eyes open (Figure 4). Fragments of this pattern mimicked wicket rhythm over the right parietal area (Figure 5). The EKG channel did not show arrhythmia or morphological changes of QRS complex during unusual electrographic events.
The interesting EEG pattern observed in this case shows several characteristics of subclinical rhythmic electrographic discharge of adults as described in 1981 (Westmoreland and Klass 1981). Sensitivity to hyperventilation, topographic distribution of rhythmic activity, non-evolving nature of frequency, gradual disappearance of rhythmicity after hyperventilation (two to three minutes after hyperventilation), and the patient's unaltered level of consciousness were helpful in the positive identification of SREDA. Though morphology and rhythmic onset of this pattern shared some characteristics of rhythmic temporal theta of drowsiness (RTTD), it was ruled-out by the topographic distribution and sensitivity to hyperventilation of the pattern. Apart from minor fluctuations of background activity, no definite epileptiform abnormalities were noted in this wakeful record. Unfortunately, a sleep record could not be obtained. The patient's brain magnetic resonance imaging (MRI) was normal.
Certain atypical electrographic features lead to confusion in the identification of SREDA in this case. Most important was the asynchronous onset when it first appeared during hyperventilation over the right parietal area with subsequent spread to the left hemisphere after about seven seconds. This electrographic progression mimics EEG characteristics of a secondarily generalized partial seizure with a right parietal onset (Figure 2). However, the patient's responsiveness and conscious level were assessed in a timely manner, which ruled out a possibility of subclinical seizure including sensory disturbances which may be seen in association with parietal lobe seizures. Subsequent recurrences of this pattern were noted to be bisynchronous but at times with an asymmetry between the hemispheres (more prominent over the right). Other atypical features were fragmentation of rhythmic pattern (Figures 5 and 6) and attenuation with eye opening on one occasion (Figure 7). Absence of long runs of SREDA in this case could be due to poor concentration in hyperventilation while the patient was being assessed with queries, simple arithmetic, eye opening, and wiggling of fingers (to rule out mu rhythm). Short fragments of SREDA, lasting for fraction of seconds with unchanged topography and frequency, resembled wicket spikes. Interestingly, a single episode of SREDA during this EEG recording was aborted with eye opening. This could be a response to eye opening or a coincidence of spontaneous termination of rhythmic activity.
Notched (bifid morphology) waveforms along with the SREDA components could be due to superimposed fast background activity over theta rhythm. In this record, rhythmic activity consisted of upper theta/lower alpha frequency (1 to 8 Hz) in contrast to the typical 5 to 7 Hz theta reported in the initial description of SREDA by Westmoreland and Klass (1981). Typical and atypical features of SREDA presented in this case are described in Table 1.
Though it is difficult to establish specific steps to identify SREDA because of its wide range of varieties, the following points should be considered:
* Any unusual paroxysmal rhythmic activity (regardless of its topography, frequency, or duration) in any patient undergoing an EEG study should be subjected to close observation.
* It is important for the technologist when he/she observes any rhythmic EEG activity to rule out a subclinical seizure by means of checking the alertness and responsiveness of the patient in a timely manner during the activity.
* If the patient has a normal sensorium and free of other clinical manifestations, one should suspect the presence of benign variants.
* SREDA almost always resembles a subclinical EEG seizure discharge. The hallmark of SREDA is its non-evolving frequency and unaltered background unlike seizure discharges. Onset and termination may be abrupt or gradual. One can expect a widespread distribution of the activity with a parieto-posterior temporal dominance.
* Another important feature of SREDA is its sensitivity to hyperventilation and prevalence in older subjects. Hyperventilation can be repeated after a reasonable time to reproduce SREDA.
* SREDA can be differentiated from RTTD which are usually confined to temporal area, occur in brief runs, and are precipitated by drowsiness. SREDA should also be differentiated from central mu rhythm which is attenuated by wiggling of contralateral fingers. Drug induced and artifactual rhythmic activity should be ruled out.
These are general guidelines and the actual identification of SREDA in real time may be in accordance but not limited to the above comments. It is also important to be aware of the atypical variants of SREDA.
REPORTED SREDA CHARACTERISTICS
Subclinical rhythmic electrographic discharge of adults is a rare distinctive EEG pattern primarily seen in older people, usually above 50 years. The term SREDA was coined by Westmoreland and Klass in 1981 when they described a series of 65 adult patients with this peculiar EEG pattern. A number of typical electrographic features of SREDA were proposed by the authors. Atypical or unusual features of SREDA were reported by the same authors in 1997 consisting of variations in frequency, topographic distribution, morphology, duration, and stage of alertness. Thus, a wide spectrum of this rare benign EEG activity has been revealed.
During polysomnography (PSG) of a middle aged man, SREDA was identified in the form of delta waves evolving to theta while the patient was in rapid eye movement (REM) sleep (Fleming et al. 2004). As it can occur in any stages of sleep, PSG professionals should be aware of SREDA and its variants. SREDA should not be mistaken for seizure activity and it may be advisable to review suspicious epochs in a chart speed of 30 mm/sec with synchronized video.
Occurrence of SREDA has been reported in two children (10 and 11 year old females) (Nagarajan et al. 2001).
In a large retrospective study in Western Ontario including 35,249 EEGs, SREDA occurred in 0.07% (Santoshkumar et al. 2009). An earlier study from Mayo Clinic revealed a prevalence of 0.04% (Westmoreland and Klass 1997). In contrast, a recent study from Kyoto reported a higher incidence of SREDA (1.2%) in a smaller cohort where only a total of 340 EEGs were reviewed (Begum et al. 2006). Higher incidence of SREDA (1%) was noted in a total of 701 EEG recordings of geriatric patients (age 84.6 ± 6.4 yrs) (Nguyen et al. 2010). The highest prevalence of SREDA is reported in the age group of 46 to 55 years (Westmoreland and Klass 1981, Westmoreland and Klass 1997, Miller et al. 1985, Santoshkumar et al. 2009). Interestingly, most of the reported cases of SREDA came from developed countries. A comprehensive study on the prevalence of benign variants conducted in a developing country did not detect SREDA among 1778 EEGs reviewed (Radhakrishnan et al. 1999). No other studies from developing countries pertaining to prevalence of SREDA are available.
Based on identification of this rhythmic activity in elderly individuals and patients with cardiovascular diseases, researchers proposed a vascular etiology for SREDA (Naquet et al. 1961, Naquet et al. 1965). They found that this pattern can be reliably reproduced by hyperventilation, nitrogen inhalation, and carotid artery compression which all produce cerebral hypoxia. SREDA has maximum amplitude over the vascular watershed areas between anterior, middle, and posterior cerebral arteries in the parietal lobe and was of longer duration after vigorous hyperventilation, which may suggest some association between vascular supply and SREDA (Zumsteg et al. 2006). Hyperventilation resulted in mild relative hypoxia due to cerebral vasoconstriction and decreased cerebral blood flow in susceptible individuals. Functional imaging studies during hyperventilation showed, up to 50% decrease in global cerebral blood flow resulting in a transient state of relative cerebral hypoxia in certain older individuals (Posse et al. 1997, Mäkiranta et al. 2004). This change in cerebral blood flow is considered as the precipitating factor of SREDA during hyperventilation. Similarly, certain cardiovascular disorders may result in poor cerebral perfusion and leads to the relative hypoxia within the territory of the affected blood vessels. This could be the triggering factor of SREDA in older individuals with cardiovascular diseases which is consistent with the vascular hypothesis posed by Naquet et al. in 1961 and Naquet et al. in 1965.
SREDA has been observed in patients with many different neurologic and nonneurologic complaints without any statistically significant increase in the number of patients with cardiovascular disorders (Westmoreland and Klass 1997). A single photon emission computed tomography (SPECT) study performed during a focal SREDA did not find any changes compared to baseline data (Thomas et al. 1992). Fast Fourier transform and time-frequency mapping demonstrated that SREDA showed little spatial and temporal correlation in contrast to the non-SREDA discharges (O'Brien et al. 1998). In the same study, Laplacian montages showed maximal activity of SREDA over parietal or parietocentrotemporal regions, whereas it was maximal in the temporal or frontotemporal regions in the non-SREDA discharges. These reports provide further evidence that SREDA is not an epileptic activity. SREDA can occur in patients with various acute brain dysfunctions followed by a favorable clinical outcome. SREDA was also observed to disappear in follow-up EEGs in two patients (Begum et al. 2006). Brigo et al. (2010) reported SREDA in a patient with transient global amnesia, in whom EEG was performed after an acute phase of the neurological event. The authors reported that this could be incidental and a relation between transient global amnesia and SREDA seemed unlikely.
Finally, a diagnostic pitfall has been reported in which a patient with nonepileptic seizures was vigorously treated with multiple antiepileptic drugs due to misinterpretation of SREDA (Brower et al. 1995). The authors cautioned that asymmetric and fragmented SREDA may mimic ictal and interictal epileptiform abnormalities, which if misinterpreted, may lead to erroneous treatment.
EEG remains the primary tool in the investigation of patients with epilepsy. The accurate interpretation of the EEG requires not only an appreciation of abnormal epileptiform activity but the ability to recognize patterns that may appear to be epileptiform but are benign in nature. Though a number of factors such as techniques of EEG recording and patient demographics may influence the prevalence of benign variants in general, misinterpretation and unawareness also should be considered as some of the major factors for the lower incidence of SREDA in the non-developed countries. Subjective variations in the EEG interpretation and a lack of well established EEG reporting system (such as coding system of Mayo Clinic) may also contribute to this. It is obvious that timely intervention of the technologist has an important role in the identification of typical and atypical SREDA which could otherwise mislead an electroencephalographer who is blind to the actual recording scenario. EEG/PSG technologists and interpreters should be aware of the typical and atypical features of SREDA and its wide spectrum. SREDA and its atypical presentations should be published to provide a continuing awareness and vigilance about the possible pitfalls in EEG interpretation.
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Rajesh P. Poothrikovil, R. EP T., RPSGT, DNT, B.Sc.1;
Abdullah Al Asmi, M.D., FRCP(C)2;
Arunodaya Gujjar, MBBS, DM3
1 Department of Clinical Physiology
2 Neurology Unit of Department of Medicine
Sultan Qaooos University Hospital
Muscat, Sultanate of Oman
3 College of Medicine and Health Sciences
Sultan Qaboos University
Muscat, Sultanate of Oman