generalized slowing

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.

Mild

Moderate

Severe

Focal slowing

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.

The "irdas"

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.

breach activity

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).

Attenuation & Discontinuity

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.

Excess beta

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.

triphasic waves

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.