Epilepsy & Behavior 20 (2011) 254–256

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Epilepsy & Behavior

j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / ye b e h

Review Article

Intermittent rhythmic delta activity patterns

Francesco Brigo ⁎
Department of Neurological, Neuropsychological, Morphological and Movement Sciences, Section of Neurology, University of Verona, Verona, Italy
Policlinico G. Rossi, Verona, Italy

a r t i c l e i n f o a b s t r a c t

Article history: Intermittent rhythmic delta activity is a typical EEG pattern that was originally described by W.A. Cobb in
Received 3 November 2010 1945 (J Neurol Neurosurg Psychiatr 1945;8:65–78). It may be classified into three distinct forms according to
Revised 15 November 2010 the main cortical region involved on the EEG: frontal (FIRDA), temporal (TIRDA), and occipital (OIRDA)
Accepted 15 November 2010
intermittent delta activity. This article is a review of the main aspects of these patterns, with a special focus on
Available online 26 January 2011
EEG features and problems that may be encountered during interpretation of these patterns. In contrast to
Keywords:
FIRDA and OIRDA, TIRDA is highly indicative of ipsilateral pathology. OIRDA and TIRDA are highly correlated
Intermittent rhythmic delta activity with epilepsy, whereas FIRDA is a rather nonspecific EEG pattern.
FIRDA © 2010 Elsevier Inc. All rights reserved.
OIRDA
TIRDA

1. Introduction artery migraine [9,10], corticobasal degeneration and progressive

Intermittent rhythmic delta activity is a typical EEG pattern
originally described by Cobb in 1945 [1]. It may be classified into
three distinct forms based on the main cortical region involved on the
EEG: frontal (FIRDA), temporal (TIRDA), and occipital (OIRDA)
intermittent delta activity. This article reviews the main aspects of
these patterns, with a special focus on EEG features and problems that
may be encountered during their interpretation (Fig. 1).
2. Frontal intermittent rhythmic delta activity
Intermittent rhythmic delta activity prevalent over frontal regions is
known as FIRDA. FIRDA was initially described by Cobb in 1945 [1],
although the term was coined by van der Drift and Magnus in 1959 [2].
This activity is characterized by transient intermittent rhythmic slow
waves with a frequency of 1.5 to 4.0 Hz localized mainly over
frontopolar regions [3]. In contrast to OIRDA, FIRDA occurs in adulthood.
This typical EEG pattern was initially attributed to deep or midline
cerebral lesions resulting from increased intracranial pressure, although
it was later described in association with several other structural and
metabolic encephalopathies. This pattern is not necessarily related to
deep midline lesions and can be associated with tumors of the posterior
fossa and third ventricle [4,5], subcortical lesions [6], cerebral edema [7],
metabolic encephalopathy caused by uremia and liver failure [8], basilar
⁎ Department of Neurological, Neuropsychological, Morphological and Movement
Sciences, University of Verona, Piazzale L.A. Scuro, 37134 Verona, Italy. Fax: + 39
0458124873.
E-mail address: dr.francescobrigo@gmail.com.
supranuclear palsy [11], Creutzfeld–Jacob disease [12–14], and demen-
tia with Lewy bodies [15,16].
FIRDA may also be recorded in otherwise normal subjects during
hyperventilation [17], and is probably secondary to functional changes
induced by hypocapnia [18]. This EEG pattern is not likely to be epileptic
in nature, although it may be associated with epileptiform activity in less
than 2% of patients. Kubota and Ohnishi [19] conducted a study to
evaluate the clinical correlations of FIRDA among patients with epilepsy.
They concluded that patients with 1.5- to 2.5-Hz FIRDA were older and
partial epilepsy was most common, compared with patients with 3-Hz
FIRDA, who were younger and had idiopathic generalized epilepsy.
In a retrospective study, Watemberg et al. [20] suggested that FIRDA
may occur during mild to moderate metabolic impairment (often renal
failure and hyperglycemia) in awake patients with previous structural
brain injury (most commonly diffuse and localized ischemic lesions). A
recent prospective study [21] found a relatively high prevalence of
FIRDA (6%), with encephalopathy and structural brain lesions being
independently related to this EEG pattern. No specific etiology of
encephalopathy associated with FIRDA was determined, although renal
failure was frequently reported. FIRDA was also observed with cortical
and deep tumors, strokes, and other focal brain lesions and, thus, was
not associated with specific cerebral locations.
The origin and significance of this activity are still unclear. FIRDA was
initially considered a projected rhythm originating from subcortical,
deep midline structures, although subsequently it has been suggested
that this pattern may reflect a pathological hyperactivity occurring in
diffuse gray matter disease, in both cortical and subcortical locations
[22,23], whereas polymorphic irregular localized delta activity occurs in
focal white matter lesions or in thalamic lesions [24].

1525-5050/$ – see front matter © 2010 Elsevier Inc. All rights reserved.
doi:10.1016/j.yebeh.2010.11.009
 F. Brigo / Epilepsy & Behavior 20 (2011) 254–256
Fig. 1. Frontal intermittent rhythmic delta activity (FIRDA) in a 76-year-old woman with intraventricular hemorrhage. FIRDA consists of a run of synchronous, rhythmic 1.5-2 Hz
delta waves with a bifrontal preponderance.
3. Temporal intermittent rhythmic delta activity
Intermittent rhythmic delta activity prevalent over temporal
regions is known as TIRDA. TIRDA was originally described by Reiher
et al. [25]. It is characterized by short trains of ≥3 seconds of
intermittent, rhythmic, saw-toothed or sinusoidal, 1- to 4-Hz activity
of 50–100 μV in amplitude, recorded predominantly over the anterior
temporal regions [25,26], and occurring more frequently during
drowsiness and light sleep. When occurring bilaterally and indepen-
dently, TIRDA may vary from side to side and is often associated with
anterior temporal spikes or sharp waves (interictal epileptiform
discharges), particularly during sleep [25].
This pattern was initially considered indicative of complex partial
epilepsy, particularly originating from temporal lobe [26–28]. A
straight correlation between short (1–6 seconds) TIRDA with a spike
focus and mesiotemporal atrophy assessed by volumetric MRI has
been reported [27,29].
Although TIRDA was initially thought to be related to extratemporal
epilepsy [28], later studies did not confirm this, suggesting that this
pattern might be considered an EEG marker of an epileptogenic zone
involving the mesial structures of the temporal lobe [30]. As a
consequence, in contrast to FIRDA and OIRDA, TIRDA is highly indicative
of ipsilateral pathology. It also has great diagnostic specificity and high
positive predictive value for mesial temporal lobe epilepsy [25]. It may
therefore be considered an interictal potentially epileptogenic pattern
possibly with the same epileptogenic significance as temporal lobe spike
or sharp-wave discharges.
Persistent polymorphic delta activity over the temporal region is
usually due to a focal structural brain injury and should be dif-
ferentiated from TIRDA, as it may not be potentially epileptogenic.
4. Occipital intermittent rhythmic delta activity
Occipital intermittent rhythmic delta activity was originally de-
scribed in patients with absence seizures by Cobb in 1945 [1]. This typical
EEG pattern occurs almost exclusively in children. Initially, this EEG
pattern was considered the occipital equivalent of FIRDA, the different
location being an age-related expression of the same pathophysiological
process [1,31] which depends on maturational factors. Hyperventilation
255
induces slow activity that is posterior dominant in children and anterior
dominant in adults, thus reflecting maturational changes. Something
similar is thought to occur with OIRDA in children and FIRDA in adults
[32]. It was later suggested that OIRDA is probably an epileptiform
interictal pattern frequently associated with primary generalized
epilepsy [33], such as generalized tonic–clonic and absence seizures
[32,34], and with localization-related epilepsy [32,35]. The high
correlation with epilepsy makes OIRDA more similar to TIRDA than to
FIRDA [32]. However, OIRDA is not pathognomonic of epilepsy, as it has
also been reported in juvenile Huntington's disease [36], central nervous
system salmonellosis [37], and subacute sclerosing panencephalitis [35].
OIRDA must be differentiated from phi rhythm. Phi rhythm, which
was described by Belsh et al. [38] as “posterior rhythm slow activity after
eye closure,” is a brief (1–3 seconds), paroxysmal, bisynchronous
occipital delta rhythm that includes at least three monomorphic delta
waves within 2 seconds of eye closure on at least two occasions during
electroencephalography [39]. It has a frequency of 2 to 4 Hz and an
amplitude of 100 to 250 μV. Although its EEG features resemble those of
OIRDA, it differs because it is triggered by eye closure and because it is
not associated with epilepsy, unless a spike component is present. The
mechanism underlying the phi rhythm is unclear, but it has been
suggested that such a rhythm may originate from subcortical regions
[39].
Conflict of interest statement
There is nothing to disclose.
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