Outside of classic epileptiform activity, EEG can show a broad array of abnormalities due to underlying focal or generalized cerebral dysfunction. Most common among these is slowing, such as from a tumor or bleed. Slowing is categorized in several ways, including generalized vs focal, continuous vs intermittent, and polymorphic vs monomorphic/rhythmic. Other abnormalities discussed here include discontinuity, asymmetry, attenuation, and breach.
Recall that when reading the background, you should look for a clear PDR, AP gradient, synchrony, symmetry, continuity, reactivity, and clear wave morphology. If any of these things are lacking in a tracing, it is said to be disorganized. Disorganization goes in hand with generalized slowing, a nonspecific finding suggestive of diffuse cerebral dysfunction / encephalopathy as can be seen with severe infections, medication or substance abuse, or neurodegenerative disease. Generalized slowing can be categorized into mild, moderate and severe. The exact delineation from one to the next is somewhat subjective, but a few rules of thumb may help.
Mild generalized slowing is typically marked by the presence of a slowed PDR and a poor AP gradient, often with excess theta admixed with the normal alpha activity throughout; reactivity, variability and the other markers of a normal awake EEG remain. With moderate generalized slowing the PDR is very fragmented or gone entirely, and the record is often predominantly theta into delta activity with much less alpha. Severe generalized slowing is highly disorganized and often discontinuous without reactivity or appreciable architecture such as an AP gradient or PDR, and is usually predominated by low amplitude delta activity.
This tracing is marked by a mildly slow PDR of 6-7 Hz, along with a notably less organized AP gradient. Much of the usual architecture of a normal study is here though, including eye blinks and variability across the page. We see some excess theta admixed into the normal and expected alpha activity, but no major delta activity. The area marked by a purple arrow may appear to be frontal delta activity, but these are in fact epileptiform spike and slow waves (note the notch-like spike before each large slow wave), discussed in the epileptiform activity section.
While generalized slowing suggests diffuse brain dysfunction, focal slowing is typically evidence of a structural abnormality involving the slowed area, particularly if the slowing is mostly delta.
Slowing is categorized in several ways. First, it can be persistent/continuous or intermittent. Continuous slowing is suspicious for a larger lesion such as a tumor, bleed, ischemic infarct or demyelinating lesion. Intermittent slowing can also be any of these things, but more often suggests a smaller lesion such as focal cortical dysplasia or the beginnings of a small tumor, and thus is more likely seen on EEG with certain state changes, overlying illness, or medication effect (this is not a hard and fast rule).
When considering any slowing, break it down into being either Slowing can be either continuous or intermittent and either polymorphic or monomorphic/rhythmic. Polymorphic slowing is most commonly seen and is thought to arise from a mix of white and grey matter injury but is generally nonspecific in etiology, while monomorphic/rhythmic slowing is thought to localize more to grey matter but, more importantly, is often concerning for epileptiform activity.
Continuous/persistent focal slowing is suggestive of a significant structural abnormality such as tumor, bleed, ischemic infarct or demyelinating lesion. While slower frequencies (delta vs theta, for instance) don't necessarily suggest a worse underlying abnormality, continuous slowing is worse than intermittent, and a rule of thumb is that the less reactive and variable a slowed region is, the worse the underlying cerebral dysfunction.
Intermittent focal slowing can also arise due to a structural abnormality, but such abnormalities tend to be smaller in nature, such as a focal cortical dysplasia or the beginnings of a small tumor, and thus are more likely seen on EEG with certain state changes, overlying illness, or medication effect (this is not a hard and fast rule).
On the example below, note how the left hemisphere (maximal temporally) continuously has a slower to at times absent PDR compared to the right, and is marked by theta to delta activity while the right hemisphere has normal alpha and beta activity.
This tracing shows persistent high amplitude delta slowing over the left hemisphere. Given the high amplitude particularly over the parasagittal chain, this may represent not just slowing but breach, which is seen after brain surgery and discussed more below. Note also the periods of mu rhythm--the resting alpha frequency of the sensorimotor cortex that is arch-like in morphology, over the right parasagittal chain; mu rhythm goes away with thoughts of or initiation of movement.
When focal slowing is seen as intermittent rhythmic delta activity, its significance varies by the region of the brain involved, with some locations suggesting epileptic potential and others just nonspecific encephalopathy. In order to be categorized as rhythmic activity, there must be 6 cycles of the activity; for example, one wave per second for 6 seconds, or two waves per second for 3 seconds. This is also discussed in the rhythmic activity section of the epileptiform activity page.
Frontal intermittent rhythmic delta activity (FIRDA) is prognostically similar to generalized slowing in that it suggests cerebral dysfunction of nonspecific etiology, and is commonly seen in very sick and encephalopathic patients, and those with dementia. On the example below note that the bifrontal delta activity does not travel back to the posterior regions; if it did, it would not be frontal but rather generalized rhythmic delta activity (GIRDA).
While FIRDA is nonspecific, temporal intermittent rhythmic delta activity (TIRDA) is considered an epileptiform abnormality with high risk for seizures from the affected temporal lobe(s); see the epileptiform activity section for details.
Somewhere in the middle, prognostically speaking, of TIRDA and FIRDA is occipital intermittent rhythmic delta activity (OIRDA), which is far, far more common in children and while often seen in kids with epilepsy can also be found in those with encephalopathy of varying etiologies. In the example below note that the OIRDA has some embedded spikes (see epileptiform activity section); in cases such as this, you should definitely consider this pattern to be epileptogenic.
This tracing shows intermittent runs of approximately 3 Hz delta activity over the left temporal region, more prominent in the anterior than posterior temporal region. Because these intervals of 3Hz delta last at least 2 seconds, they complete the 6 cycle requirement for rhythmic delta activity. Note that the delta is very apparent in the lateral temporal leads below the traditional parasagittal and temporal chains--a reminder to always keep an eye on all of your available chains on EEG.
Breach activity describes higher amplitude, often spiky and irregular appearing activity over a region of the skull that has been previously opened due to brain surgery. It is so named because it arises due to the breach in the skull.
Often, breach activity coincides with slowing because the region of brain underneath, if it needed surgery, likely had something wrong with it in the first place. It is important not to mistake the spiky appearance of breach activity for epileptiform discharges, although it is common that epileptiform activity is embedded within breach (again, abnormal brain that led to the necessary surgery may be irritable and thus with epileptiform activity).
Recall that when assessing background you should look for a PDR, AP gradient, synchrony, symmetry, continuity, reactivity, and clear wave morphology. On this page, we have a continuous tracing that is synchronous and symmetric. However, there are only fragments of a PDR on both sides, and when present it is no faster than 5 Hz. Thus we have at least mild generalized slowing here. However, there is also no AP gradient--realistically, the page would look much the same if we flipped it upside down. Furthermore, we don't have much alpha activity, with the page mostly theta and delta activity that is relatively monotonous in appearance from beginning to end. Overall, then, this would be considered moderate generalized slowing.
While breach activity is seen as higher than expected amplitude and spiky morphology, attenuation describes lower amplitude activity of varying causes. Persistent attenuation over a region can arise from something sitting between the brain and the skull, such as a hematoma or hygroma. A sudden regional attenuation may be evidence of a stroke. Intermittent attenuation may even be interictal or ictal, such as tonic seizures that classically involve a sudden diffuse attenuation with overriding fast activity.
Discontinuity describes intermittent periods of attenuation, and outside of the neonatal stage of life is always highly abnormal and a marker of severe generalized slowing. You may see it in comatose patients and those with severe brain injury; in cases of refractory status epilepticus unresponsive to multiple antiseizure drugs and infusions, extreme sedation leading to an intentional discontinuity called burst suppression (which requires at least 50% of the record to be suppressed) is used.
This is a complicated tracing so let's look at one side at a time. First note that on the left side you have a clear PDR of 8-8.5 Hz, which is in the normal range. However, the AP gradient on the left is poor, with excess slow activity in the frontal regions. Note also that the F7 electrode is bad (note how Fp1-F7 and F7-T3 move in exact opposition to each other, a sign of a bad F7 electrode) and Fp1 and F3 are too close to each other (they've formed a salt bridge, seeing the same voltage as each other and thus cancelling each other out on bipolar, leading to a flat line; on an average montage, they'd have identical appearing lines).
Moving to the right side, we see a persistent / continuous, somewhat low amplitude delta activity in the frontal regions, and fragments of a PDR in the occipital leads. There is even less of an AP gradient and normal morphology than on the left side. As such, we say this tracing has persistent right hemispheric polymorphic delta slowing on a background of mild generalized slowing.
Excess beta activity, when diffuse or frontally predominant, is a commonly seen phenomenon most often arising as a medication effect in the setting of benzodiazepine or barbiturate use. It is marked, as expected, by low amplitude beta overriding the normal activity throughout the tracing. It can also be seen with anxiety and, somewhat counterintuitively, with drowsiness. While excess beta is an abnormality, it is essentially a benign one.
This tracing shows a burst of generalized high amplitude delta activity at about 3Hz, lasting several seconds and thus meeting the ACNS criteria for rhythmicity (aka requires 6 cycles). The delta activity is generalized but more prominent on the right side, particularly in the temporal chains. We would thus classify this as generalized intermittent rhythmic delta activity (GIRDA) with right-sided predominance. Recall that GIRDA is similar to FIRDA prognostically in that it suggests nonspecific and diffuse cerebral dysfunction.
Triphasic waves are a nonspecific waveform most classically associated with metabolic (historically, hepatic) encephalopathy. Their name is descriptive, as they are comprised of three parts, with each part being slightly longer than the preceding one. They are most often generalized, with a subtle delay in the onset of each as you move from the anterior to posterior regions.
Sometimes, triphasics can be periodic, particularly in critically ill patients. In the example below there are several on the page, but the most well formed one is marked; note that this page also shows moderate generalized slowing.
Here we see a good PDR throughout of 10 Hz, but note while the right temporal region is alpha and beta activity, the left temporal region has a kind of "sloppier" appearance with admixed slower frequencies from theta and delta. In a normal awake adult, you should basically never see theta or delta activity. The slowing here is not rhythmic and seems to run across the entire page, so we'd classify it as focal left temporal persistent polymorphic theta to delta slowing.
Mild generalized slowing is marked by the presence of most of the normal architecture, but a slowed PDR and suboptimal AP gradient. It is commonly seen in encephalopathy patients.
With mild generalized slowing, you should see a lot of the usual artifacts of the awake state that reveal reactivity, including eye blinks.
Moderate generalized slowing usually lacks a PDR, or has only a fragmented PDR, with no AP gradient and usually dominant theta activity instead of the normal alpha.
The delineation from mild to moderate or moderate to severe can be subjective, but moderate gen slowing should still show state changes while severe gen slowing does not, and lacks the PDR that mild gen slowing should retain.
Severe generalized slowing is marked by lack of any normal architecture, poor to absent reactivity, discontinuity, and often low amplitude diffuse delta activity.
Here we see an example of severe gen slowing that is essentially invariant, unreactive, and very low amplitude.
This is a complex and highly abnormal tracing. We see severe generalized slowing with no PDR or AP gradient, bilateral and asymmetric discontinuity, and multifocal epileptiform discharges. This is actually consistent with hypsarrhythmia, discussed in the epilepsy syndromes section.
Persistent focal polymorphic slowing suggests nonspecific underlying dysfunction as can be seen from a tumor, stroke, bleed or other parenchymal injury. Here we see persistent slowing over the left hemisphere, maximal temporally.
This continuous right anterior quadrant (the anterior temporal and frontal regions) polymorphic delta slowing may seem subtle at first but note how similar delta activity is not over the left frontal regions. When slowing is subtle it can help to look at it from farther away, to better see the gestalt.
Be sure to always look at the entirety of the tracing. Here, you may be distracted by the relatively symmetric posterior portion of the right temporal chain and overriding generalized slowing, but don't miss the mid-temporal slowing as compared to the left temporal chain.
Here we see continuous albeit subtle theta to delta slowing over the left temporal chain, but there is also a more prominent period of polymorphic delta slowing broadly through the temporal region.
The entire right hemisphere is slowed in this example, but if you look closely the left anterior quadrant is also slightly slowed, although this is easily missed because you don't have a normal contralateral side to compare.
Again we see bilateral frontal slowing here, which can make t hard to initially pick up because there isn't a clear asymmetry to which the eye is drawn. Just remember that the frontal leads should be predominantly fast activity such as beta and alpha; here, we see too much frontal theta.
Frontal intermittent rhythmic delta activity (FIRDA) is a nonspecific marker of diffuse cerebral dysfunction, and is commonly seen in very ill, encephalopathy, or neurodegenerative patients. Note that the delta activity here does not move far posteriorly.
Generalized intermittent rhythmic delta activity (GIRDA) is similar to FIRDA in that it suggests nonspecific and diffuse cerebral dysfunction. With any of the IRDAs, it is important to ensure that you don't see embedded spikes or notches, which would make them to epileptiform in nature.
Temporal intermittent rhythmic delta activity (TIRDA) differs from the other IRDAs in that it is essentially always considered epileptogenic, and shoudl be thought of as a form of interictal activity.
Occipital intermittent rhythmic delta activity (OIRDA) is much more commonly seen in children, in whom it is often but not always associated with epilepsy.
FIRDA is not always as clean cut as the prior example, as seen here where, while retaining an approximately 1 Hz activity, there are fluctuations and a somewhat sloppy appearance the frontal waveforms.
Discontinuity, or periods of attenuation in between periods of higher amplitude activity, is always abnormal after the neonatal period, and is a hallmark of severe generalized slowing.
This tracing is perhaps most notable for the fact that it is read at the standard sensitivity of 7uV/mm, but looks essentially flat. As such, this shows diffuse and very severe attenuation without much physiologic activity.
In cases of very refractory status epilepticus, it may necessary to "reboot" the brain via extreme sedation. In these cases, you use EEG to titrate that sedation burst suppression, aka intentional discontinuity marked by bursts of activity in between essentially flat periods of attenuation. You may see this pattern non intentionally in patients after severe cardiac ischemia or other causes of coma.
This shows a disorganized, mostly theta background, consistent with moderate generalized slowing. We also see some triphasic waves: generalized up-down-up discharges in which each phase is slightly longer than the last, with a slight lag going from anterior to posterior.
Triphasics, being a marker of encephalopathy, are often seen in ICU patients with other signs of diffuse brain dysfunction, be it generalized slowing or, as seen here, intermittent rhythmic delta activity with frontal predominance (FIRDA).
Triphasics exist on one end of a wide spectrum of abnormal activity, with clear epileptiform discharges on the other end. So, sometimes along with triphasics you'll see activity that is suspicious but not clearly epileptiform in nature.
This tracing shows diffuse and very prominent excess beta activity, captured shortly after administration of high dose lorazepam to stop a prolonged seizure.
Again we see excess beta diffusely here, but in this tracing it is admixed with a lot of myogenic artifact, which is too fast to be cerebral in etiology from scalp EEG.
Breach activity is a sequelae of brain surgery, due to the residual skull defect. Breach is marked by sharper / spiky appearing waves that are often higher in amplitude than those in the non-breach areas. Underlying rhythms such as Mu or wickets are more apparently seen.
Breach and slowing don't have to go together, but often do simply because if you are getting a craniotomy, there's likely something wrong with the brain tissue underneath the area of that craniotomy.