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Encephalopathic EEG Patterns
Introduction
Alterations in attention, cognition, or consciousness are clinically characteristic of encephalopathy. This diffuse cerebral dysfunction can vary in severity due to numerous etiologies, including toxic, metabolic, infectious, and degenerative derangements. Acute encephalopathy may range from mild confusion and delirium to coma, typically presenting with a fluctuating course that involves altered mental status, confusion, and changes in motor activity. Symptoms often include lethargy, cognitive impairment, altered memory and information processing, and disturbed sleep-wake cycles. In more chronic, slowly progressive, or static encephalopathies, initial attentional retention may be followed by a loss of cognitive capacity.[1][2]
Encephalopathy is typically observed in older adults and is commonly seen in intensive care units and in postoperative individuals. Despite the new developments in intensive medical care, acute encephalopathy is still a significant cause of morbidity and mortality in hospitalized patients. In this regard, electroencephalography (EEG) enables rapid bedside electrophysiological monitoring, providing dynamic real-time information on neocortical brain activity and dysfunction.[1]
EEG is useful for evaluating patients with acute and chronic encephalopathies. The primary role of EEG in this setting is to rule out seizures as a cause of altered mental status. Various patterns can be observed in patients with encephalopathy; abnormal patterns, especially those with an acute-to-subacute onset, are sensitive for encephalopathy but not specific for diagnosing its causes. Most encephalopathies are associated with the slowing of dominant rhythms and background activity. This is most likely due to the involvement of both the cortical neurons and the subcortical white matter dysfunction. Overall, EEG is useful for assessing the extent of cerebral dysfunction in encephalopathy and for monitoring changes in association with clinical progression.
A review of EEG emphasized that it is not pathognomonic of encephalopathy or encephalitis. However, when interpreted correctly and within the clinical context, some phenotypes may reflect specific pathophysiology, such as lateralized periodic discharges in herpes simplex virus-1 infection, generalized periodic discharges in sporadic Creutzfeldt-Jakob disease, and extreme delta brushes in anti-N-methyl-D-aspartate receptor autoimmune encephalitis. Specialist guidelines include EEG for disease assessment, monitoring, and prognostication in hepatic, cancer immunotherapy, viral, prion, autoimmune encephalitis, and hypoxic-ischemic encephalopathy. EEG also plays a crucial role in confirming or excluding nonconvulsive seizures or status epilepticus, especially among those who are critically ill, and in understanding recent concepts like epileptic encephalopathy and the ictal-interictal continuum.[3]
Function
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Function
Electroencephalogram
EEG is typically requested to assess brain electrical activity and to correlate findings with physiological and disease states. While primarily used to rule in or rule out seizures, it can also aid in diagnosing encephalopathy and nonepileptic spells. Standard EEGs typically last 30 to 60 minutes but may be extended depending on the patient’s clinical status and initial findings. Patients with persistent altered sensorium often undergo prolonged EEG with video monitoring to facilitate timely and accurate assessment of encephalopathic states.[4][5]
The usual EEG recording in the laboratory lasts at least 20 minutes, uses 19 active electrodes, and includes rest periods, stimulation procedures, a 3-minute hyperventilation period, and intermittent photic stimulation. Meanwhile, bedside recording uses at least 8 electrodes, and the stimulation procedures, EEG duration, and the need to repeat the examination depend on the indication. Furthermore, simultaneous video recording is recommended.[6] In modern neurocritical care practice, continuous EEG monitoring is increasingly utilized for encephalopathic patients, particularly those at risk of nonconvulsive seizures or status epilepticus. This enables dynamic assessment of brain function over 24 to 48 hours and improves early detection of evolving patterns, prognostication, and monitoring of therapeutic responses.[7]
The EEG background activity varies with age:
Children (<8 years old):
- Posterior dominant rhythm is slower than in adults.
- Faster beta frequencies appear over frontal regions.
- Slower waveforms are observed posteriorly.
- Minimal theta (4–8 Hz) activity during wakefulness with no delta activity.
Adults (>8 years old):
- Posterior dominant rhythm of 8.5 to 12 Hz in relaxed wakefulness.
- Rhythm attenuates with eye-opening and returns with closure.
- An anterior–posterior gradient is present.
During drowsiness and sleep:
- Theta activity increases, especially centrally and parasagittally.
- Nonrapid eye movement (NREM) sleep: delta activity predominates.
- Rapid eye movement sleep: alternates with NREM and shows mixed frequency activity.[8]
The video and EEG recordings allow the reviewer to access and review any clinical events and their associated waveforms in a time-locked fashion to determine if they are associated.[9] The typical duration of an EEG in encephalopathic patients is longer than that of a routine outpatient EEG. Encephalopathic patients are usually seen in acute hospital settings and typically require a longer-duration EEG of at least 24 to 48 hours to fully assess and understand the condition. This also helps in monitoring their progress and assessing for nonconvulsive status epilepticus.[10][11][12] Longer-duration, continuous EEG monitoring has been shown to improve detection rates of subclinical seizures, guide escalation of antiseizure therapy, and help prognosticate outcomes in critically ill patients.[7][13]
Issues of Concern
Characteristic EEG Patterns Encountered in Acute Encephalopathy
Diffuse slowing
Diffuse slowing of background frequencies is a common EEG finding in acute encephalopathy. The degree of slowing correlates with impairment in attention and consciousness, often beginning with posterior-dominant rhythm slowing and reduced frontal beta activity, then progressing to increased theta and delta activity as severity worsens.[14][15] An exception to reduced beta is drug-related cases, in which fast beta activity may be abundant (eg, benzodiazepines or barbiturates).[16] As encephalopathy progresses, theta- and delta-band activity increases, initially appearing intermittently and subsequently becoming continuous. In comatose states, delta activity predominates and slows further as the coma deepens. Additional changes include loss of reactivity and the emergence of a discontinuous background with a burst-suppression pattern.
As severity increases, interburst intervals lengthen, ultimately progressing to an isoelectric (flat) tracing. This stage is called electrocerebral inactivity or electrocerebral silence.[17] Diffuse slowing is a common finding in anti-N-methyl-D-aspartate (NMDA) receptor encephalitis in children and pediatric acute liver failure with encephalopathy, as seen in case reports.[18][19] Clinically, diffuse slowing reflects global network dysfunction from metabolic, hypoxic-ischemic, septic, or toxic causes and is nonspecific. Trend evolution—such as worsening delta, discontinuity, or loss of reactivity—is more informative than a single snapshot. Continuous EEG enhances detection of these changes in the intensive care unit, aids early recognition of nonconvulsive status epilepticus, and guides treatment decisions. Key interpretive points include: assessing state-dependent reactivity and background variability; identifying superimposed periodic or rhythmic patterns (eg, generalized rhythmic delta activity/generalized periodic discharges) that may affect management; and integrating medications, temperature, and sedation levels before inferring prognosis.[3][7][20]
Triphasic waves
Triphasic waves (TWs) are characterized by a broad, blunt waveform with a positive–negative–positive morphology, typically maximal over the frontal regions with an anterior–posterior phase lag. They often occur in a periodic pattern of up to 2.5 Hz and may have a generalized distribution.[21] Historically, TWs were strongly associated with hepatic encephalopathy and were once considered pathognomonic for the condition. They were also linked to stages of encephalopathy progression and elevated ammonia levels. However, subsequent studies demonstrated that TWs can also occur in other metabolic disturbances, including renal failure, sepsis, and toxic encephalopathies, as well as in structural lesions causing diffuse network dysfunction.[21][22] TWs are often stimulus-sensitive, appearing or becoming more prominent with stimulation or state changes, typically overriding a slow background activity.[23][24]
Functional imaging and source modeling have shown that these discharges arise from large bilateral cortical networks involving the frontal and temporopolar regions, consistent with impaired consciousness and cognitive dysfunction observed in affected patients.[25] Differentiating features include stereotyped morphology, lack of evolution in frequency or field, and improvement with correction of the underlying metabolic disturbance rather than antiseizure therapy.[20] In critically ill patients, the presence of TWs often reflects more severe underlying brain dysfunction. When accompanied by background attenuation or burst suppression, they are associated with poorer neurologic outcomes.[26][3] Early recognition of this pattern enables clinicians to promptly address the underlying cause and avoid unnecessary escalation of antiseizure therapy.
Generalized rhythmic delta activity
Generalized rhythmic delta activity (GRDA), previously referred to as frontal intermittent rhythmic delta activity (FIRDA), is a 2 to 3 Hz rhythmic or semirhythmic high-amplitude activity with anterior predominance.[27][28] Historically, FIRDA was considered an indicator of midline structural lesions, such as third ventricular tumors, but it is now recognized as a nonspecific EEG finding in encephalopathic states. FIRDA is associated with encephalopathic states due to various etiologies like toxic, metabolic, infectious, neoplastic, and epileptic entities. Studies of FIRDA have reported a transient, rhythmic slow-wave pattern over the anterior EEG leads, observed across a wide range of cerebral lesions and metabolic disturbances. Furthermore, FIRDA is more commonly associated with the neurocritical care setting than with outpatient EEG clinics. In patients with stroke, the involved vascular territory may also contribute to FIRDA generation.[29]
GRDA with posterior predominance, often called occipital intermittent rhythmic delta activity (OIRDA), is more common in children, classically in absence epilepsy.[30] A recent case series identified an atypical pattern of OIRDA on the EEGs of patients with self-limited focal epilepsies, including childhood epilepsy with centrotemporal spikes and Panayiotopoulos syndrome. Beforehand, OIRDA was identified as a symmetric sinusoidal occipital-maximal activity, often associated with childhood idiopathic generalized epilepsies. However, it was also reported along with other physiologic or pathological entities like focal epilepsy. In this case series, OIRDA, without a prominent field effect, was lateralized or maximal on the hemispheric side ipsilateral to the more prominent epileptiform discharges in these focal epilepsies. These waves also displayed a notched morphology because of the intermixed sharp wave activities, even if the sharp waves are not happening repetitively.[31]
Lateralized rhythmic delta activity (LRDA) is more strongly associated with seizures than frontally predominant GRDA, which is usually benign. Accurate recognition is important to distinguish these patterns from benign rhythmic variants such as phi rhythm, slow alpha variants, subclinical rhythmic electrographic discharges of adults (SREDA), or hyperventilation-induced slowing. Furthermore, Angelman syndrome and NMDA receptor antibody encephalitis can also produce morphologically distinct patterns of RDA.[28] Clinically, GRDA and FIRDA reflect diffuse or deep midline network dysfunction rather than focal cortical hyperexcitability. These patterns are often reactive, non-evolving, and improve with correction of the underlying etiology. In the intensive care unit, their presence indicates moderate-to-severe encephalopathy but does not necessarily predict seizures in the absence of other high-risk EEG features.[20]
Lateralized Periodic Discharges or Periodic Lateralized Epileptiform Discharges
Lateralized periodic discharges (LPDs) (historically Periodic Lateralized Epileptiform Discharges “PLEDs”) consist of lateralized sharp waves or spike–slow-wave complexes at roughly 1 to 3 Hz occurring in a semirhythmic, periodic pattern without clear evolution or spread. They are most often associated with acute or subacute focal structural lesions, with stroke being the most common etiology. Still, they also occur with tumors, infections (eg, herpes simplex virus encephalitis), autoimmune/inflammatory processes, and other focal injuries.[32][33][34] Whether LPDs represent seizures remains debated and appears context- and morphology-dependent.[35]
In a retrospective cohort, LPDs were linked to subsequent epilepsy in about one-third of patients and to markers of epileptogenicity in roughly 18%.[36] More recent work shows that EEG features modify seizure risk: sharply contoured LPDs, superimposed fast activity, or superimposed rhythmicity carry progressively higher seizure risk than blunt delta-morphology LPDs, which carry the lowest risk. Imaging–EEG studies also show ipsilateral acute focal abnormalities with similar frequency in LRDA and LPDs, underscoring a shared focal pathophysiology.[37]
Meanwhile, case reports mentioned other conditions that have been recognized as the underlying pathology for PLEDs, namely alcohol withdrawal, Creutzfeldt-Jakob disease, anoxic brain injury, and hemiplegic migraine. Also, the increasing utilization of continuous video EEG in the acute care setting of the ictal-interictal continuum (IIC) has revealed that LPDs and other periodic and rhythmic patterns are extremely common. Reviews have been conducted to address the ongoing debate that LPDs and the pattern lying along the IIC are called "periictal," which means that LPDs are temporally associated with epileptic seizures (although not necessarily in the same recording).
The following criteria were proposed to determine which kind of LPDs should be considered as representing interictal/irritative brain injury versus ictal/periictal LPDs:
- Spiky or sharp LPDs followed by associated slow after-waves or periods of flattening, giving rise to a triphasic morphology, should be included in the definition of LPDs-plus.
- In its subtype, the "LPDs-max" pattern pertains to an ictal pattern and, therefore, a focal nonconvulsive status epilepticus, sometimes related to the subtle motor signs and epileptic seizures. LPDs-max consists of periodic polyspike-wave activity and focal burst-suppression-like patterns. LPDs-max also have a posterior predominance over the temporoparietooccipital regions and are refractory to antiseizure drugs.[33][38][39][40][33][41]
Generalized Periodic Epileptiform Discharges and Bilateral Independent Periodic Epileptiform Discharges
Generalized periodic epileptiform discharges (GPEDs) and bilateral independent periodic epileptiform discharges (BIPLEDs) are commonly seen in settings of severe diffuse cerebral dysfunction, most notably in anoxic or hypoxic brain injury after cardiac arrest.[42][43] EEG findings, combined with clinical examination and neuroimaging, are often used to help determine prognosis in hypoxic encephalopathy post-cardiac arrest. GPEDs have long been regarded as a “malignant” EEG pattern, strongly associated with poor neurological outcomes, including persistent coma and high mortality, particularly in post-anoxic injury.[44] Recent case reports emphasize that BIPLEDs in EEGs are commonly caused by anoxic encephalopathy and central nervous system infections. They are also associated with coma and high mortality and are thus markers of poor prognosis.[45] Rarely, reversible metabolic or infectious etiologies can present with GPEDs and a more favorable course, so clinical context, background reactivity, and timing after the insult are critical.[3]
Extreme delta brush
Extreme delta brush (EDB) is characterized by rhythmic 1 to 3 Hz delta activity with superimposed, time-locked beta “brush” activity over the delta up-phase, typically bifrontal or frontocentral in distribution and relatively stimulus-insensitive. In the American Clinical Neurophysiology Society framework, this pattern is classified as a periodic discharge with a “+F” (superimposed fast) modifier.[20] EDB is highly associated with anti-NMDA receptor encephalitis and, when present, strongly supports the diagnosis in the appropriate clinical context. While its sensitivity is limited, ranging from 20% to 35%, its specificity for autoimmune encephalitis is high; however, rare cases have been reported in other autoimmune conditions, such as dipeptidyl-peptidase-like protein 6 encephalitis.[46][47][48]
The presence of EDB has been correlated with greater disease severity, higher rates of intensive care unit admission, and worse functional outcomes, including increased mortality in some cohorts.[46] Recognition of this pattern should prompt early immunotherapy and close neurologic and critical care monitoring to improve outcomes. When evaluating EDB, it is essential to confirm that the superimposed fast activity is truly time-locked to the delta rhythm rather than representing an artifact. Clinicians should assess the background reactivity and continuity, as well as the presence of coexisting EEG patterns such as GRDA or seizure activity, which can influence prognosis. Importantly, the absence of EDB does not exclude NMDA receptor encephalitis, as many patients may instead display only diffuse slowing or GRDA.[47]
Alpha coma and spindle coma
Diffuse alpha-frequency activity (8–13 Hz) is observed in comatose states. When the alpha activity is posteriorly predominant and shows variability or reactivity to noxious stimuli, the coma may result from brainstem lesions, and this pattern is typically associated with a poor prognosis.[49] More diffuse, nonreactive alpha activity is most often observed following anoxic injury after cardiac arrest, also correlating with poor outcomes. Prognosis depends on both the underlying etiology and the presence of EEG reactivity, with more favorable outcomes in toxic-metabolic encephalopathies and worse outcomes in anoxic encephalopathies.[49][50] Spindle coma consists of paroxysmal bursts of 11 to 14 Hz activity appearing on a delta background and is usually known to occur in cases of anoxic injury, intracranial hemorrhage, diffuse cerebral insults, and head trauma.[51][52] EEG pattern spindle coma is associated with the involvement of the pontomesencephalic junction.[53]
A recent study analyzed EEGs from patients with COVID-19 and examined disease severity, respiratory failure, immune and metabolic dysfunction, sedation status, and neurological examination. The results revealed that the majority of patients experienced severe encephalopathy, and some had alpha coma. Disease severity, sedation, immune, and metabolic dysfunction were not different between those with alpha coma and those without. The comparatively high incidence of the rare alpha coma pattern may reflect direct severe acute respiratory syndrome coronavirus 2 neurotropism with preference to the brainstem ascending reticular system. The study concluded that systematic early EEG monitoring for encephalopathy associated with severe COVID-19 is important for acute care and the management of long-term neurological and cognitive sequelae, and may help elucidate the pathophysiology.[54]
Burst suppression
Burst suppression is characterized by alternating periods of high-voltage activity (bursts) and periods of very low or absent activity (suppressions) lasting at least 50% of the recording.[20] When this pattern occurs after anoxic brain injury, it is considered a malignant EEG pattern associated with very poor neurological outcomes, particularly when the bursts are stereotyped, nonreactive, or progressively decrease in frequency.[55] In contrast, burst suppression observed under controlled conditions, such as therapeutic anesthesia or induced hypothermia, is often reversible and carries less prognostic weight.
Other literature has described burst-suppression EEG patterns as intermittent high-power, broad-spectrum oscillations alternating with isoelectricity during general anesthesia, hypothermia, coma, and early infantile encephalopathy. Burst suppression is characterized by bursts of high-voltage, slow, sharp-wave activity, alternating with periods of background suppression in the EEG. If induced by deep anesthesia or encephalopathy, burst suppression is bihemispheric and often seen as a nonepileptic phenomenon.[56][57] The clinical context is essential for interpretation. Burst suppression accompanied by epileptiform activity or periodic discharges is associated with a higher risk of seizures and reflects more extensive cerebral dysfunction—the presence or absence of reactivity and the evolution of the background over time further influence prognostic assessment.[58]
Electrocerebral inactivity or electrocerebral silence
Electrocerebral inactivity is defined as an EEG pattern with no electrical activity exceeding 2 μV when recorded from scalp electrodes properly placed according to the International 10-20 system and using a standard amplifier setting.[20] This pattern is most commonly seen in the context of severe anoxic-ischemic brain injury, irreversible coma, or brain death. According to the American Clinical Neurophysiology Society and the American Academy of Neurology guidelines, confirming electrocerebral inactivity requires strict technical standards—including a minimum of 30 minutes of high-quality recording, appropriate electrode impedances, sensitivity settings, and environmental controls—to rule out artifact. Electrocerebral inactivity must be distinguished from low-voltage recordings due to metabolic suppression, hypothermia, or technical error.[20][59]
In the setting of post-anoxic brain injury, electrocerebral inactivity strongly correlates with the futility of neurological recovery and is considered a highly malignant pattern. In brain death protocols, electrocerebral inactivity is 1 of the accepted ancillary tests in jurisdictions where the EEG is used to support the determination of brain death.[59][60] Among newborns, the utmost caution is indicated since electrocerebral inactivity can be observed in the absence of cerebral death.[57]
Clinical Significance
Encephalopathy is commonly described as an alteration of consciousness or attention ranging from mild to severe, with severe cases potentially leading to poor prognosis or death. Secondary to various etiologies, encephalopathy can manifest as acute or chronic. EEG is typically requested to assess for pattern and rhythm abnormalities, which may or may not be associated with ictal states, and continuous monitoring is also used to assess for progression and response to treatment. Narrative reviews have focused on acute symptomatic seizures occurring among patients with electrolyte disturbances. Seizures are more commonly seen among those with sodium disorders such as hyponatremia, hypocalcemia, and hypomagnesemia. These seizures do not entail a diagnosis of epilepsy but are classified as acute symptomatic seizures. EEG has limited specificity in distinguishing between various electrolyte disturbances. The distinct EEG feature slows normal background activity; however, other EEG findings may also occur, including epileptiform abnormalities.[61]
The following section provides a more detailed discussion of EEG findings in common acute encephalopathies.
Hepatic Encephalopathy
- This is encountered in patients with liver failure or insufficiency from any cause. Recent reviews mentioned minimal hepatic encephalopathy (MHE) as the earliest form of hepatic encephalopathy, which can affect up to 80% of patients with liver cirrhosis. Also, MHE affects daily functioning, quality of life, driving, and overall mortality. Spectral analysis of EEG and quantitative analysis of sleep EEG provide early markers of cerebral dysfunction in patients with cirrhosis with MHE.[62]
- The EEG changes at the beginning commonly include slowing of the posterior dominant rhythm, followed by a gradual slowing of the background, with the appearance of theta- and delta-band activity.[14] FIRDA can appear even in the presence of the posterior dominant rhythm.
- Classic TWs are best observed when encephalopathy worsens and ammonia levels are elevated. As severity increases, sleep architecture becomes sparse.[15]
- Bursts of well-formed, smoothly contoured, negative-positive-negative, bilateral, symmetrical, synchronous, regular, reactive, periodic or rhythmic, 1.5 to 2.0 Hz, frontocentral, triphasic complexes with frontooccipital lag meet the criteria for typical TWs and are highly suggestive of toxic-metabolic encephalopathies, frequently hepatic, uremic, or sepsis-associated encephalopathies with multi-organ failure.
- EEG aids in early detection, prognostication, and treatment monitoring in hepatic encephalopathy, with continuous EEG helping identify secondary contributors such as nonconvulsive seizures.[3]
Renal (Uremic) Encephalopathy
- Retention of uremic solutes, alterations in neurotransmitter balance (eg, increased glycine, decreased GABA and glutamine), and blood–brain barrier dysfunction contribute to the pathogenesis of uremic encephalopathy and correlate with EEG abnormalities such as generalized slowing and triphasic-wave patterns.[63]
- High-voltage rhythmic delta activity with bilateral spike-slow-wave complexes is often observed in patients with dialysis disequilibrium syndrome, characterized by obtundation after a dialysis session.[64]
- These events may or may not be associated with clinical seizures.[65][66]
- In patients with end-stage renal disease (with or without diabetes), EEG background slowing (increased delta/theta activity) was significantly associated with renal dysfunction and comorbidity burden.[67]
Hypocalcemia
- Hypocalcemia is, by definition, a corrected total serum calcium level below 2.2 mmol/L. Decreased calcium levels are most commonly associated with vitamin D deficiency and hypoparathyroidism, among several other etiologies.[68]
- A study of 22 patients with hypocalcemia secondary to hypoparathyroidism reported slow-wave or spike–slow-wave complexes on EEG, which can mimic epileptiform activity.[69]
- Initially, the most common EEG change is progressive slowing, with dominance of theta- and delta-frequency activity. There is also an association between generalized spikes and sharp waves and a burst of delta activity. A 3 to 4 Hz spike and wave discharges have been reported in neonatal EEG records.[70] 'Absence status' has also been reported in these patients.[71]
- Formula feeding, parathyroid hormone insufficiency, and low vitamin D are associated with neonatal hypocalcemia. Tetany and QT prolongation may occur with mild hypocalcemia, and transient EEG abnormalities can result.[62]
Hypercalcemia
- Hypercalcemia is, by definition, encountered when the serum calcium levels are above 10.5 mg/dL.[71][72] This derangement is usually seen in patients with renal failure, hyperparathyroidism, and malignancies with an invasion of bony structures.
- The EEG background changes with increased theta- and delta-band activity when serum calcium levels exceed 13 mg/dL.[14] The EEG can also show spikes and sharp waves. With an even further increase in calcium levels, background slowing increases primarily in the frontal regions, accompanied by a paroxysmal burst of theta- and delta-band activity and TWs.[73][74]
- Association with diffuse and more posterior occipital spike and slow-wave activity has also been reported, suggesting a posterior reversible encephalopathy syndrome-like presentation with hypercalcemia.[75][76]
- Case reports also identified hypercalcemia as the cause of a subacute syndrome of progressive dementia and marked changes in the EEG, such as bursts of 1.5 to 2 Hz intermittent rhythmic delta activity superimposed on a low-voltage background activity in the EEG. Clinical and EEG abnormalities rapidly resolved after serum calcium levels returned to normal. The reports also recommended obtaining serum calcium levels and EEGs to detect a Creutzfeldt-Jakob disease-like syndrome in the setting of hypercalcemia.[77]
Hypoglycemia
- Hypoglycemia is typically defined as a blood glucose level below 70 mg/dL. The correlation between blood glucose level, consciousness or attention level, and EEG changes is highly variable across individuals.[78]
- The lowest blood glucose level at which detectable EEG changes may be observed is 29 to 40 mg/dL.[79]
- The blood glucose threshold for hypoglycemia is slightly higher in individuals with diabetes, at which EEG changes can be observed.[80]
- A common finding associated with lower glucose levels is slowing of background activity, primarily in the theta frequency range. This is noted in both adults and children.[81]
- In those in the intensive care unit with hypoglycemic coma, malignant EEG patterns such as nonreactive background with periodic or burst-suppression activity are strongly associated with poor outcomes, while preserved EEG reactivity correlates with a favorable prognosis.[82]
Hyperglycemia
- With milder hyperglycemia, the EEG background activity may slow slightly or remain unchanged. As glucose levels increase, diffuse delta slowing increases, and when a level of approximately 400 mg/dL is crossed, a sporadic spike can be observed.
- Epilepsia partialis continua, clinically defined as a syndrome characterized by continuous jerking of a body part, commonly a limb, is strongly associated with nonketotic hyperglycemia, focal spikes on EEG, focal slow waves on EEG, and a slower background.[83][84]
- Elevated fasting glucose levels are associated with reduced EEG functional connectivity, and in hyperosmolar states, continuous EEG may detect cerebral dysfunction before overt neurological deterioration and clinical seizures.[85]
Hypernatremia
- Older adults and infants are more likely to develop neurological symptoms and EEG abnormalities when serum sodium levels exceed 160 mmol/L.[86][87]
- EEG changes in hypernatremia are characterized by diffuse slowing of the background activity.[88]
- In pediatric post-cardiac surgery patients, hypernatremia was independently associated with worse EEG background abnormalities, higher incidence of seizures, and more severe magnetic resonance imaging brain injury.[89]
Hyponatremia
- EEG changes in hyponatremia are associated with background slowing in the theta-to-delta frequency range as serum sodium levels decline, typically below 116 mg/dL.
- The EEG may be characterized by a stimulus-induced paroxysm of delta activity and central high-voltage theta activity at 6 to 7 Hz.[90] TWs and lateralized periodic discharges have also been reported.[91]
- Absence status epilepticus with focal EEG discharge activity has also been reported to be associated with hyponatremia.[92][93]
Hypothyroidism
- EEG in hypothyroid states is commonly associated with low-voltage activity, predominantly in the theta frequency range. Comatose individuals in this condition may show diffuse suppression with minimal activity. Sporadically, periodic sharp waves may be encountered.[94]
Hyperthyroidism
- EEG changes in hyperthyroidism include an increased alpha activity with prominent central beta activity. An anterior sporadic burst of theta or delta activity has been described.[95] TWs have been noted as well.[96]
- In acute thyrotoxicosis, the EEG is characterized by spikes and sharp waves with paroxysmal delta activity, often associated with clinical seizures, as described.[14][97]
Hashimoto Encephalopathy
- This is a chronic, relapsing autoimmune thyroid disorder associated with antithyroid antibodies and often occurs alongside other autoimmune diseases, such as systemic lupus erythematosus and rheumatoid arthritis, which are typically steroid-responsive.
- EEG is associated with generalized slowing and FIRDA in these patients. Often, TWs are also seen.[98]
- Recent studies show that common neuropsychiatric features of Hashimoto encephalopathy include consciousness disturbance and psychosis, followed by cognitive dysfunction, involuntary movements, seizures, and ataxia. EEG abnormalities and decreased cerebral blood flow on single-photon emission computed tomography (SPECT) are frequent findings. Clinical phenotypes can include acute encephalopathy, chronic psychiatric presentations, limbic encephalitis, progressive cerebellar ataxia, and a Creutzfeldt-Jakob disease–like form.[99]
Hypoxic and Anoxic Encephalopathy
- Anoxic or hypoxic injury commonly follows cardiac arrest, with EEG findings ranging from mild background slowing to severe suppression. Poor prognostic patterns include alpha or spindle coma with absent reactivity, burst suppression with prolonged interburst intervals, and electrocerebral inactivity or silence.[14][44] Results from recent studies link EEG evolution after hypoxic injury to underlying synaptic dynamics, whereby an early excitation–inhibition imbalance, driven by preferential excitatory synaptic failure, produces suppression or burst suppression patterns.[100]
- Hypoxic-ischemic encephalopathy in neonates is associated with a favorable outcome if the EEG performed within the first 8 hours after birth shows an active, normal background and portends a poorer outcome if the background activity is grossly abnormal or inactive.[101] Another study mentioned that neonates with hypoxic-ischemic encephalopathy with burst suppression, low voltage, and flat trace in the EEG most accurately forecast long-term neurodevelopmental results.[102]
Infections Associated with the Central Nervous System
- Central nervous system infections, such as encephalitis, cerebral abscess, meningoencephalitis, or meningitis, can manifest with diffuse changes and focal findings on EEG.
- Viral encephalitis, particularly herpes simplex virus, often shows periodic lateralized epileptiform discharges, focal slowing, and high-voltage spike–wave activity in the temporal regions, with generalized slowing and epileptiform discharges also frequently observed.[103]
- Autoimmune encephalitis (eg, anti-NMDAR): EEG commonly demonstrates generalized slowing, epileptiform activity, and the characteristic “extreme delta brush” pattern.[104]
- West Nile virus encephalitis: EEG typically shows generalized slowing with anterior predominance, along with focal slowing or epileptiform discharges, particularly in the frontotemporal regions.[105]
- Neurosyphilis: Temporal epileptiform discharges, sometimes in the form of lateralized periodic discharges, are more common than in viral encephalitis.[106]
- Zika virus encephalitis: EEG may demonstrate diffuse background disorganization, focal slowing, epileptic discharges, generalized spike–wave complexes, or periods of voltage attenuation. No specific EEG pattern is diagnostic.[107]
- Other central nervous system infections (bacterial, fungal, parasitic): EEG findings are generally nonspecific and include generalized or focal slowing, periodic discharges, and epileptiform activity.[108]
Trauma and Intracranial Hemorrhage
- Traumatic brain injuries (TBI) can be associated with focal and diffuse changes based on the injury's extent and the affected intracranial structures. Global damages like diffuse axonal injury are typically associated with diffuse slowing, whereas contusions and hemorrhages are associated with focal slowing and epileptiform discharges.[109][110]
- In extreme TBI cases, different EEG patterns can be encountered, including alpha or spindle coma due to brainstem injury, burst suppression, and even electrocerebral inactivity.
Drug-Induced or Toxic Encephalopathy
- The etiology of this type of encephalopathy is numerous. The EEG changes in this setting can range from the diffuse slowing of the background in theta and delta frequency activity to an abundance of superimposed beta activity, especially with benzodiazepine and barbiturate overdoses.
- Some drugs (eg, lithium) are associated with focal, multifocal, or diffuse epileptic activity and seizures as well.
- TWs are also seen in drug-induced encephalopathies.[15]
Other Issues
EEG in Chronic Encephalopathies
Chronic encephalopathies can also show EEG changes. The most common finding is slowing of background activity in the theta and delta bands as the encephalopathy, or disease, worsens. In neurodegenerative conditions like Alzheimer, Pick, or Parkinson disease, and vascular dementia, EEG findings are typically normal at the initial stages.[111][112][113][114] A low-amplitude EEG background activity is common in Huntington disease.[115] Periodic complexes with very high amplitude 2 to 4 delta waveforms intermixed with epileptiform or sharp discharges appearing every 5 to 7 seconds are seen in subacute sclerosing panencephalitis. Clinically, these complexes can be associated with myoclonic jerks.[116]
Creutzfeldt-Jakob Disease
Creutzfeldt-Jakob disease (CJD) is a rapidly progressive neurodegenerative disorder associated with the prion protein, an abnormal isoform of a cellular glycoprotein. Most patients with CJD typically die within 1 year of contracting the illness. Clinically, in addition to rapidly progressive dementia, there can be myoclonus, visual or cerebellar signs, pyramidal/extrapyramidal signs, and akinetic mutism with variable association. EEG changes are commonly observed in this condition and are characterized by diffuse slowing, periodic complexes, and GRDA.[117] The periodic complexes in CJD are more frequent, typically occurring at 1 Hz. These complexes typically contain a sharp, slow wave and may initially be unilateral, becoming bilateral as the disease progresses.[118] Moreover, the EEG pattern in CJD is characterized by diffuse abnormal activity, although lateralization to 1 hemisphere has been reported in the early stages of the disease. The abnormal EEG activity in CJD is diffuse without clear spatial predominance in anterior or posterior brain regions.[119]
EEG Changes in Encephalopathy Associated with COVID-19 or SARS-CoV-2 Infection
Common EEG changes in patients with COVID-19-related encephalopathy include generalized slowing of the background.[120][121][122] In another cohort of 18 patients, there was a direct correlation between oxygen saturation and EEG changes at presentation. Lower oxygen levels were associated with more severe EEG patterns, such as the association with epileptiform discharges.[123] Another cohort of 15 patients with COVID-19-related encephalopathy, comprising 873 patients admitted for SARS-CoV-2 infection, reported relatively homogeneous EEG changes, primarily characterized by diffuse background activity, slowing, and loss of reactivity to external stimulation. Two patients in this cohort were comatose from anoxic injury, with 1 case associated with a suppressed background and the other with a discontinuous activity consistent with postanoxic status epilepticus.[124]
A recent study reported EEG findings in both COVID-19 survivors and nonsurvivors who had an EEG either due to seizure or encephalopathy. Of the 1468 patients who were COVID-19-positive, only 19 underwent an EEG. Among the 13 survivors, the most common EEG finding was normal, followed by mild diffuse slowing; however, among the 6 nonsurvivors, the most common EEG finding was moderate-to-severe slowing in 50% of patients. From this, it can be concluded that COVID-19 infection does not increase the propensity for epileptiform discharges on EEG.[125]
Enhancing Healthcare Team Outcomes
The recognition and management of encephalopathic EEG patterns in critically ill individuals depend on seamless interprofessional collaboration within the neurocritical care team. Neurologists and intensivists play a central role in identifying and interpreting abnormal EEG findings, integrating these results with clinical status, imaging, and laboratory data to guide rapid decision-making.[3] EEG technologists ensure accurate electrode placement, high-fidelity recordings, and continuous monitoring—especially vital in unstable patients at risk for nonconvulsive seizures or status epilepticus.[1] Intensive care unit (ICU) nurses serve as the team’s frontline, closely monitoring neurological status, ensuring airway protection and sedation titration, and promptly communicating clinical changes to the treating team. Pharmacists contribute by adjusting antiseizure, sedative, and vasoactive medications to optimize both EEG quality and patient safety.[6]
Interprofessional coordination in the ICU setting allows for early detection of evolving EEG patterns, enabling rapid intervention before irreversible neurologic injury occurs.[3][7] Standardized communication protocols, real-time EEG reporting, and multidisciplinary rounds help align treatment goals, minimize delays in care escalation, and improve patient outcomes.[1] By integrating EEG data with clinical and hemodynamic parameters, the neurocritical care team can individualize management strategies, prevent complications, and enhance recovery potential. This collaborative approach strengthens diagnostic precision, optimizes resource utilization, and supports evidence-based critical care for patients with encephalopathy.[1][3][6][7]
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