Diffuse EEG Abnormalities



Diffuse EEG Abnormalities


Thoru Yamada

Elizabeth Meng



General Features of Diffuse EEG Abnormalities

Any clinical condition that causes clouding of consciousness is usually accompanied by diffuse EEG abnormalities. The degree of impaired consciousness is categorized as follows:



  • Delirium is characterized by a severe degree of confusion with disorientation to time, place, and/or person. The patient may be restless and hyperkinetic with psychic symptoms including incoherence, hallucinations, and delusion.


  • Confusion is a state in which there is a mild reduction in the level of consciousness. The patient with a defect in attention span reacts normally to ordinary stimulation but is disoriented to time, place, and/or person.


  • Lethargy or hypersomnia is a severe degree of drowsiness in which the patient can be awakened with ordinary stimulation but may fall back to sleep as soon as the stimulus is removed.


  • Stupor or semicoma is a state of partial loss of response in which the patient can be temporarily aroused with vigorous stimulation but lapses into an unresponsive state when not stimulated.


  • Coma is defined as a state of complete or almost complete loss of consciousness from which the patient cannot be aroused, even by powerful stimuli.

More detail in degree of consciousness can be measured by a Glasgow Coma Scale.1 It is based on three measures: (1) eye opening (E), (2) verbal response (V), and (3) motor response (M). The scales are 1 to 4 for E where 4 is spontaneous and 1 is none, 1 to 5 for V where 5 is normal conversation and 1 is none, and 1 to 6 for M where 6 is normal and 1 is none. Using the Glasgow Coma Scale, the overall degree of impaired consciousness can be categorized as severe for GSC 3 to 8, moderate for GCS 9 to 12, and mild for GCS 13 to 15. (For children who are too young to have reliable language skills, modified scales can be used for verbal response.)

Diffuse cerebral dysfunction could be secondary to metabolic, toxic, or inflammatory illnesses, and demyelinating or degenerative diseases. EEG can provide an objective measure of severity of these pathological processes. It can also aid in prognostication. EEG changes are, however, rarely specific for the diagnosis. Nevertheless, the EEG assists to narrow down the diagnostic possibilities when combined with appropriate clinical information.

Diffuse EEG “slowing” can be categorized into three basic patterns:



  • Background slowing without accompanying theta or delta slow waves (Fig. 11-1)


  • Diffuse theta and delta activity associated with normal background activity (Fig. 11-2)


  • Slow background activity along with diffuse theta and delta activity (Fig. 11-3)

In general, slowing of background activity implies cortical dysfunction. Delta-theta slow waves signify white matter disease. Delta-theta slow waves, along with slow background activity, represent dysfunction of both the cortex and the white matter.

The degree of diffuse EEG abnormalities correlates fairly well with the level of consciousness. EEG grades can be classified as follows:

Grade IA: Mild slowing of background activity (7 to 8 Hz) without significant increase of theta-delta slow waves (Fig. 11-4A)

Grade IB: Moderate slowing of background activity (4 to 6 Hz) without significant increase of theta-delta slow waves (Fig. 11-4B)

Grade IIA: Dominant theta activity with some delta slow waves associated with normal or near-normal background activity (Fig. 11-5A)

Grade IIB: Dominant theta activity with some delta slow waves associated with slow background activity (Fig. 11-5B)

Grade IIIA: Dominant delta activity associated with normal or near-normal background activity (Fig. 11-6A)

Grade IIIB: Dominant delta activity associated with slow background activity (Fig. 11-6B)

Grade IVA: Moderate to high-amplitude (>50 µV) delta activity with minimal or no background activity (Fig. 11-7A)

Grade IVB: Low-amplitude (<50 µV) delta activity with minimal or no background activity (Fig. 11-7B)

Grade VA: Burst suppression pattern with suppression period of less than 5 seconds (Fig. 11-8A)

Grade VB: Burst suppression pattern with suppression period of greater than 5 seconds (Fig. 11-8B)

Grade VIA: Near electrocerebral inactivity (Electro-Cerebral Inactivity or ECI) (Fig. 11-9A and B)

Grade VIB: ECI (Fig. 11-9C and D)







FIGURE 11-1 | An example of slight slowing of waking background activity (7 to 8 Hz) without significant increase of delta-theta slow waves. This is grade IA abnormality.






FIGURE 11-2 | An example of excessive irregular diffuse delta slow waves associated with normal 9- to 10-Hz alpha rhythm. This is grade IIA abnormality.







FIGURE 11-3 | An example of slow background activity (5 to 7 Hz) associated with diffuse delta-theta slow waves. This is grade IIB abnormality.






FIGURE 11-4 | A: Grade IA with slight slowing of background activity (7 to 8 Hz) without significant delta-theta slow waves. B: Grade IB with moderate slowing of background activity (6 to 7 Hz) without significant delta-theta slow waves.







FIGURE 11-4 | (Continued)






FIGURE 11-5 | A: Grade IIA with background activity of mostly alpha rhythm associated with interspersed theta-delta slow waves. B: Grade IIB with background activity of 5 to 6 Hz associated with mixture of theta-delta slow waves.







FIGURE 11-5 | (Continued)






FIGURE 11-6 | A: Grade IIIA with irregular delta slow waves, associated with a fair amount of alpha background activity. B: Grade IIIB with irregular delta slow waves, associated with slow background activity consisting of 5- to 7-Hz theta activity.







FIGURE 11-6 | (Continued)






FIGURE 11-7 | A: Grade IVA with high-amplitude prominent, irregular delta slow waves with minimal alpha or theta background activity. B: Grade IVB low-amplitude irregular delta slow waves with minimal or no alpha or theta background activity.







FIGURE 11-7 | (Continued)






FIGURE 11-8 | A: Grade VA EEG represents burst suppression pattern with burst duration of 1 to 2 seconds and suppression period of 0.5 to 1 seconds. B: Grade VB EEG with prolonged suppression period of more than 5 seconds and short burst duration.







FIGURE 11-8 | (Continued)






FIGURE 11-9 | Grade VIA with markedly depressed EEG activity showing only very-low-voltage theta-delta activity with a sensitivity of 7. Note EKG contamination on the EEG tracings (shown by vertical lines) (A). With increased sensitivity (S = 2), however, the presence of EEG activity in between EKG artifacts becomes clear (B). C, D: Grade VIB with ECS recorded with ECS montage including long interelectrode distance at channels 1 and 2 (Fp1-O2 and Fp2-O1). With regular sensitivity (S = 7), tracings are “flat,” only showing small EKG artifacts (A). Cerebral inactivity (ECS or ECI) is verified with increased sensitivity (S = 2), only showing EKG artifacts (QRS and T waves) and intrinsic “noise” (low-voltage fast activity) (B).







FIGURE 11-9 | (Continued)







FIGURE 11-9 | (Continued)

In general, the degree of diffuse cerebral dysfunction correlates with the above grades, progressively worse from grade I to VI, and B is worse than A within the same grade.

In grade I, the EEG shows only slight slowing of alpha rhythm, and consciousness may not be altered. As the degree progresses to II, the patient may be awake but may be slow in responding or somewhat lethargic. At grade III, the patient is likely to be stuporous, but external stimuli shows reactive EEG changes with increased faster-frequency activity. In some cases, stimulus brings out slower activity with generalized highvoltage delta bursts, which is termed paradoxical arousal response (see Fig. 6-19). As delta activity becomes more dominant, correlating clinically with a semicoma or coma state, there will be less reactive EEG changes when stimulated. In addition to slowing of the background activity and increased theta-delta slow wave activity, some diffuse EEG abnormalities may also include paroxysmal activity like sharp waves, theta, delta bursts, or spike discharges. Grade IV or V is usually associated with a comatose state. The patient may show a reactive EEG change to external stimulus in grade IV but usually not in grades V or VI. In evaluating the course of the disease process, serial EEGs are useful. An example of this progressive EEG improvement is shown in Figure 11-10A-D. The frequency change is more reliable than the amplitude change; slower-frequency and lower-amplitude delta waves are worse than faster-frequency and higher-amplitude delta activity. Spontaneously fluctuating EEG patterns (e.g., alternating theta-delta dominant pattern and alpha-theta dominant pattern) or the presence of reactive EEG to external stimuli suggests a better prognosis than those of nonreactive, relentless EEG. Despite close correlation between the degree of EEG abnormality and the level of consciousness, EEG change may precede clinical deterioration of mental status. Conversely, EEG improvement may lag during the process of clinical recovery.


EEG Patterns that Reflect Diffuse Cerebral Dysfunction

Other than diffuse slowing, there are some EEG patterns that characterize the EEG abnormalities in relation to diffuse encephalopathy. They are triphasic waves, frontal intermittent rhythmic delta activity (FIRDA) (frontally predominant GRDA*) or occipital intermittent rhythmic delta activity (OIRDA) (occipitally predominant GRDA*), periodic patterns, burst suppression pattern, alpha-theta coma, spindle coma, and ECI.


TRIPHASIC WAVES

Triphasic waves consist of an initial small negative sharp discharges followed by large positive sharp discharges with subsequent negative wave. The typical triphasic pattern of more or less continuous, stereotyped waveforms was classically described in patients with hepatic coma2 (Fig. 11-11; see also “Hepatic Encephalopathy” in this chapter). Atypical triphasic patterns consisting of less continuous and less stereotyped waveforms may be seen in other toxic-metabolic encephalopathies (i.e., uremic encephalopathy, anoxic encephalopathy, lithium toxicity, and other metabolic derangements) (Fig. 11-12).3,4,5,6,7 Triphasic waves usually occur in patients with



a mild to moderate impairment of consciousness but may also be seen in fully awake patients. Some triphasic discharges secondary to encephalopathy are difficult to differentiate from nonconvulsive status epilepticus (see Figs. 8-17 and 10-33B; see also Fig. 13-1B and C).






FIGURE 11-10 | A 38-year-old patient with diagnosis of viral encephalitis. On admission, the patient was stuporous with EEG showing diffuse semirhythmic 1.5- to 2-Hz delta activity with no appreciable background activity (A). Within 2 days, EEG started to show improvement with faster-frequency delta activity (B). On the 5th day, EEG further improved consisting of a mixture of delta and theta activities and the patient became arousable (C). On the 7th day, patient was awake and EEG showed 7- to 8-Hz background activity mixed with some delta-theta slow waves (D).






FIGURE 11-10 | (Continued)






FIGURE 11-11 | A 54-year-old patient with diagnosis of hepatic encephalopathy secondary to cirrhosis of liver with EEG showing fairly rhythmic triphasic waves (examples are circled). Note a phase lag of the triphasic waves from the front to the back of the head.






FIGURE 11-12 | A 49-year-old patient with chronic uremic encephalopathy. EEG shows slow background activity consisting of 4- to 6-Hz theta background activity and irregular delta slow waves. Note intermittent triphasic waves (shown by circles) that were less stereotypical and less rhythmic as compared to those seen in hepatic encephalopathy (see Fig. 11-11).


FIRDA (FRONTALLY PREDOMINANT GRDA*)/OIRDA (OCCIPITALLY PREDOMINANT GRDA*)

FIRDA/frontally predominant GRDA or OIRDA/occipitally predominant GRDA can also be seen in patients with encephalopathy or seizures. This was described in detail in “Intermittent Rhythmic Delta Activity,” Chapter 8.


PERIODIC PATTERNS

Periodic patterns consist of repetitive and fairly stereotyped waveforms appearing in regular (or nearly regular) intervals. Examples are seen in Creutzfeldt-Jakob disease (CJD) (see Fig. 10-33A-D), subacute sclerosing panencephalitis (SSPE) (see Fig. 10-32A and B), and also in postanoxic cerebral insult (see Figs. 10-34B and 10-35B; see also Video 13-1). If periodic discharges occur in a focal or lateralized prominence, they are referred to as periodic lateralized epileptiform discharges (PLEDs) or (LPD* = lateralized periodic discharges) (see Figs. 10-39, 10-40 and 10-41). If they occur in a bilaterally independent fashion, they are called bilateral independent periodic lateralized epileptiform discharges (BiPLEDs) (BIPD* = bilateral independent periodic discharges) (see Fig. 10-42A and B). PLEDs are commonly seen in patients with acute or subacute, severe and focal destructive lesions such as massive cerebral infarction, acute exacerbation of a brain tumor, or herpes simplex encephalopathy. PLEDs may also be seen in patients with epilepsia partialis continua (see Video 13-8).These are described in more detail in “Periodic Lateralized Epileptiform Discharges,” Chapter 10.


BURST SUPPRESSION PATTERN

Burst suppression pattern consists of recurrent, at times periodic or pseudoperiodic, bursts associated with an EEG suppression period of variable duration. The suppression period is of either no or very-low-amplitude (<10 µV) cerebral activity (Fig. 11-8A and B; see also Fig. 10-34A and B). Burst suppression pattern may be categorized as a subset of periodic or pseudoperiodic pattern. The bursts can be a mixture of a variety of all types of waveforms including sharp, spike, alpha, beta, theta, and delta activities. The suppression period commonly lasts from 2 to 10 seconds but could be longer than 10 to 20 minutes. This is one of the reasons why an EEG recording requires a minimum of 30 minutes to determine brain death. The burst suppression pattern induced by anesthetic drugs may last as long as several hours, which can still be recovered after cessation of drugs. Burst suppression implies the deepest level of a coma state before brain death. It is commonly seen in patients with an acute and severe degree of cerebral insult, most commonly in severe anoxic encephalopathy,8,9 acute intoxication of CNS-suppressant drugs,10,11 and severe hypothermia.12 Some patients may have myoclonic twitches associated with the bursts (see Fig. 10-35A and B; also see Video 13-7).

Longer suppression periods, along with shorter duration and smaller amplitude bursts, are associated with a worse degree of cerebral insult (see Fig. 11-8A and B). Most conditions with burst suppression pattern, especially in a postanoxic cerebral insult, indicate a grave prognosis. However, recoverable burst suppression pattern can be induced therapeutically by various anesthetic agents including barbiturates,13,14 propofol,15 (see Video 11-2), etomidate,14 and isoflurane.16 A suppression period of several hours induced by deep anesthesia can be recovered.


ALPHA-COMA AND THETA-COMA PATTERN

In a coma state, EEG is expected to show diffuse, generally low-voltage slowing or burst suppression pattern. In contrast to this expectation, there is a pattern that is paradoxically represented by abundant alpha activity with little or no slow waves in comatose patients (Fig. 11-13). This pattern is termed alpha coma. The alpha activity is often diffuse or more anteriorly dominant than that seen in a normal condition. It is also nonreactive to external stimuli. This pattern is most frequently seen in severe anoxic encephalopathy and generally suggests an extremely poor prognosis.17,18 However, some studies have reported cases of recovery from alpha coma.19 Alpha coma may be a transient phenomenon in a postanoxic state.18 We have experienced a case of postanoxic encephalopathy where continuous EEG monitoring started with burst superstition pattern changing progressively to faster background activity through theta then to alpha and eventually became low-voltage pattern before death (Fig. 11-14A-D). Alpha coma has been reported in other conditions including patients with brainstem lesions limited to the pontomesencephalic level,18,20 high-voltage electrical injury,21 and Reye’s syndrome.22 Alpha coma in these conditions has a better prognosis than that of postanoxic cerebral insult.

Theta coma is analogous to alpha coma but has a slightly slower frequency than alpha coma (Fig. 11-15).23


SPINDLE COMA

Some comatose patients display a sleep pattern including spindles, vertex sharp waves, and/or K complexes mixed with theta-delta slow waves, but the patient is not arousable (Fig. 11-16; see also Fig. 8-4). This is referred to as spindle coma. This pattern has most often been described in patients with head injury24,25,26,27 and has been reported in other conditions including acute cerebral anoxia,28,29 viral encephalitis,30 thalamic or brainstem lesion,28,29 subarachnoid hemorrhage,28 and drug intoxication.28

A functional disturbance of anatomical lesions involving the midbrain, hypothalamus, or pons has been postulated for generation of spindle coma but pathological confirmation has not been made. Some coma or vegetative state patients may show diurnal EEG changes with alternating awake and sleep patterns.24

Spindle coma, especially secondary to posttraumatic coma, carries a relatively benign outcome.24,26 Reactive EEG changes including K complexes by external stimuli also suggest favorable outcomes.27,28,29,30,31 Recent review of studies has shown overall mortality of 23% in spindle coma patients compared to mortality exceeding 65% in comas associated with other EEG patterns including burst suppression, periodic pattern, and alpha-coma pattern.32 The appearance of sleep spindles following diffuse slowing during a coma or a semicoma state during long-term recording suggests improvement of cerebral function.







FIGURE 11-13 | A 52-year-old comatose patient after anoxic cerebral injury. EEG showed diffuse and bianterior dominant 10- to 11-Hz alpha activity, representing alpha-coma pattern. Some underlying delta slow waves are also seen.






FIGURE 11-14 | A 65-year-old male with postanoxic cerebral insult after cardiac arrest. The first EEG at 8 hours after cardiac arrest showed intermittent diffuse low-voltage theta interrupted by some brief suppression periods (A). EEG then showed progressively faster frequency (B) and background activity reaching alpha frequency, that is, alpha-coma state (C and D), which seemingly was improving from the earlier EEG despite Glasgow Coma state remained the same.6 EEG then changed to the low-voltage pattern when Glasgow Come Scale changed from 6 to 3 (D). The patient expired several hours after this EEG.







FIGURE 11-14 | (Continued)







FIGURE 11-14 | (Continued)






FIGURE 11-15 | A 45-year-old comatose patient following a cardiac arrest. Diffuse theta activity, representing theta-coma pattern.







FIGURE 11-16 | A 15-year-old patient after nonpenetrating head injury. EEG showed sleep spindles and K complex resembling normal sleep pattern, but the patient was not arousable. This represents spindle coma.


ELECTROCEREBRAL SILENCE (ECS) OR ELECTROCEREBRAL INACTIVITY (ECI)

The definition of brain death may differ depending on social, religious and ethical backgrounds, and traditional custom and philosophical concept. In the United States, brain death is defined as “irreversible loss of function of the brain including brainstem.”33 This can be diagnosed by clinical evaluation, which demonstrates signs of unresponsiveness, total absence of brainstem reflexes, and apnea. Before determining the brain death, reversible medical conditions that may mimic brain death must be excluded. These include hypothermia with a core temperature below 32°C (although to make an EEG “flat” in normal conditions requires 20°C or less), drug intoxication especially by barbiturate or other sedative drugs, and severe metabolic and endocrine derangements. EEG and neuroradiologic examinations are used as ancillary tests. In the United States, the ancillary tests are no longer mandatory if a clinical examination and history are solid and meet the clinical criteria of brain death. Guidelines of American Clinical Neurophysiology Society (ACNS) define ECS or ECI as “no EEG activity over 2 µV when recorded from scalp electrode pairs 10 or more centimeters apart with interelectrode impedances under 10,000 Ohm” (see Fig. 11-9C and D). The following are recommended for EEG recording for determination of ECII34:



  • A full set of scalp electrodes should be utilized: the electrodes should include Fz, Cz, and Pz. Additionally, a ground electrode is required, though double grounding should be avoided.


  • Interelectrode impedance should be under 10,000 Ω but over 100 Ω: extremely high- and extremely low-electrode impedance attenuates the potential. Extreme low impedance (<100 Ω) suggests shorting (electrodes “salt bridge”) of two electrodes.


  • The integrity of the entire recording system should be tested: this can be accomplished by observing artifacts introduced by touching each electrode.


  • Interelectrode distance should be at least 10 cm: this is to avoid a cancellation effect of short interelectrode distance, especially when dealing with extremely lowamplitude activity. Double interelectrode distances compared to routine electrode placement, for example, Fp1 to C3 (instead of Fp1-F3) are commonly used. The longest interelectrodes (Fp1-O2 or Fp2-O1) may also be included.


  • Sensitivity must be increased from 7 µV/mm to at least 2 µV/mm for at least 30 minutes of the recording, with inclusion of appropriate calibration. This is necessary to delineate low-voltage activity (Fig. 11-9C and D). A calibration signal of 10 to 20 µV is appropriate for a sensitivity of 2 µV/mm.


  • Filter setting should be appropriate for assessment of ECS: the high filter (low-pass filter) should not be below 30 Hz and the low filter (high-pass filter) should not be higher than 1 Hz. The use of the 60-Hz notch filter is allowed if necessary. One may include a low filter (highpass filter) setting of 0.3 Hz for part of the recording to enhance slow waves, but that filter is not required.


  • Additional monitoring techniques should be employed when necessary to clarify the record: this include EKG and respiration monitoring. Additional electrodes placed over the dorsum of the hand may help to monitor
    environmental electrical artifacts. If excessive EMG (muscle tone) artifacts interfere with a reliable interpretation of the EEG, the use of a short-acting muscle relaxant is allowed.


  • There should be no EEG reactivity to intense somatosensory, auditory, or visual stimuli: this can be accomplished by calling the patient’s name, pinching the nail bed, and/or delivering photic stimulation. Photic stimulation may elicit ERG (electroretinogram) at Fp1 or Fp2 but should not yield photic evoked response or driving response at occipital electrodes.


  • Recording should be made only by a qualified technologist: because ECI is recorded in an “electrically hostile” ICU setting where many electrical and mechanical pieces of equipment are attached to the patient, the EEG is often contaminated by a variety of artifacts. This is further aggravated by the increased sensitivity (gain) required for ECS determination. Identifying and eliminating artifacts that interfere with the accurate interpretation depends on the skill, knowledge, and experience of the technologist (R. EEG T.) and also of the interpreting EEGer (Electroencephalographer or clinical neurophysiologist).


  • A repeat EEG should be performed when ECI is in doubt. Before 1980, repeating the EEG 24 h after the first ECS recording was mandatory in order to determine brain death. However, accumulated evidence indicates that no patients survived for more than a short period after one EEG showed ECI.35 Therefore, a repeat EEG is no longer required for adult patients. Although this can apply to term neonates and children, an EEG cannot substitute for a neurological examination in brain death evaluation. If there is any doubt, question, or uncertainty from either a technical or clinical perspective, the EEG should be repeated after an interval, for example, of 6 hours.


  • Physiological variables and medication should be documented. This is because severe hypothermia, low blood pressure, or low oxygen saturation can cause cerebral inactivity or severe suppression EEG activity, which may be reversible by correcting these variables. Also, it is important to record all medications, especially sedative or anesthetic drugs such as barbiturates, benzodiazepine, propofol, or narcotics.

EEG or another ancillary test is also required for pediatric patients greater than 37 weeks gestational age to 18 years only when other clinical tests for determinations of brain death are not definitive or in doubt. The Task Force for Determination of Brain Death in Children36 recommends a repeat EEG 24 hours after the first ECI for newborns of 37 weeks gestation to 30 days. For age of 30 days to 18 years, 2 EEG examinations 12 hours apart are recommended.

Because of the electrically “noisy” environment in the ICU and the high sensitivity used in the recording, artifact contamination in EEG is inevitable. The most common artifact is EKG. In fact, if EKG artifact is not present in an ECI recording, the technologist should check the integrity and parameters of the recording system. At times, an exceedingly high-amplitude EKG prevents appropriate EEG interpretation. In this case, selecting or creating a different montage may reduce the artifact. Repositioning the patient’s head may also reduce EKG artifact. One may need to change the pillow or bedsheet if it has become wet.

EMG artifacts may obscure the EEG. Neuromuscular blocking agents such as pancuronium or succinylcholine can be used to temporarily eliminate EMG artifacts. Since these drugs are paralytics, they should be used only with an order from a physician and administered by a nurse.

Respiration-related artifacts, by either the ventilator itself or head movement associated with respiration, may cause rhythmically recurring artifacts in association with the respiratory cycles. The waveforms are variable depending on the cases (see Fig. 15-21A-D and also Videos 15-7 and 15-8). Sometimes, movement of fluids accumulated in the ventilator circuit may produce artifacts. The technologist may need to monitor respirations by visually observing the chest movement or by using a transducer to record the respiratory movement. It may be necessary to temporarily disconnect the ventilator circuit to verify the disappearance of the events of concern. This has to be done by the ICU nurse, respiratory therapist, or ICU physician.

Other sources of artifacts include pacemakers, warming blankets, IV pumps, and dialysis units. Also, electrostatic artifacts can be caused by movements around the bed. As in any other EEG recording, low- and equal-electrode impedances minimize the introduction of artifacts. EEG is rarely ECI if any brainstem reflex remains, especially in adults. Conversely, as high as 20% of patients who meet the clinical criteria of brain death may still show some electrocerebral activity in their EEG for several hours to several days after clinical brain death was established.37 However, the chance of long-lasting survival in clinically brain dead patients with minimal preservation of EEG activity is extremely unlikely.


Diffuse Encephalopathies Associated with Relatively Specific or Characteristic EEG Patterns

EEG is a sensitive and reliable test to evaluate the severity of cerebral dysfunction and to assess the progress of a disease process. However, most of the EEG abnormalities reflecting diffuse cerebral dysfunction are nonspecific and do not lead to a specific diagnosis. Nonetheless, there are several conditions in which the EEG shows a relatively specific or diagnostic pattern. Here, only those conditions as well as relatively common diseases in which EEG is requested are described in some detail. EEG findings in other remaining conditions are listed in Table 11-1 with reference citations.


HEPATIC ENCEPHALOPATHY

In the early stage of hepatic encephalopathy, EEG shows slowing of alpha rhythm, which is gradually replaced by theta and delta waves as the disease progresses. In the somnolent or mildly stuporous state, the EEG often shows triphasic waves (see Fig. 11-11).124 This is characterized by a small negative wave followed by a prominent positive sharp wave and subsequent broad negative wave. It appears as a “blunt spike wave” in some cases and may be difficult to differentiate from the EEG of absence status or nonconvulsive status epilepticus (see Figs. 8-17, 13-1B, and 13-12B). Finding a well-defined spike among the sharp and wave complexes indicates epileptiform activity rather than triphasic waves of encephalopathy.











TABLE 11-1 Slowing and/or Paroxysmal Discharge in Different Cerebral Disorders








































































































































































































































































































































































































































































Slowing


Paroxysmal Discharges


References


I. Metabolic Disorders





Hypoglycemia


++(D)


++(D) Spk


38,39


Hyperglycemia (nonketotic)


+(D)


+(F) Spk


40,41


Hepatic encephalopathy


++(D)


++ Triphasic


42,43


Uremic encephalopathy, acute


+(D)


+(D) Spk, triphasic waves


44,45


Uremic encephalopathy, chronic


+/-(D)


+ (D) Spk, photoparoxysmal response


46,47


Hypocalcemia (hypoparathyroidism)


++ (D)


++ (D) Spk


48


Hypercalcemia (hyperparathyroidism)


+(D)



49


Hyponatremic (water intoxication)


++ (D)


+/-


50


II. Vitamin Deficiencies





Vitamin B6 (pyridoxine) deficiency


+/-(D)


++ (D) Spk


51


Vitamin B1 (Wernicke’s encephalopathy)


+(D)



52


Vitamin B12 (pernicious anemia)


++ (D)


++ (D, F) Spk


53


III. Endocrine Diseases





Adrenocortical insufficiency (Addison’s disease)


+ (D)



54


Adrenocortical hyperfunction


Fast activity ↑



55


Hypopituitarism (Sheehan’s syndrome)


+ (D)



56


Hyperthyroidism


Fast activity ↑


+


57


Thyrotoxicosis


Fast activity ↑


+ (D) Triphasic wave


58


Hypothyroidism (myxedema)


+ (D)


+ (D) Spk


54,59


Acute porphyria


+ (D, F)


+ (D, F) Spk


60


IV. Degenerative Disorders





Tay-Sachs disease


+ (D)


++ (D) Spk, myoclonus


61,62


Cherry red spot myoclonus syndrome


+/- (D)


++ (Positive spike at vertex), myoclonus


63


Gaucher’s disease


+/- (D)


++ (D) Photoparoxysmal response


64


Globoid leukodystrophy (Krabbe’s disease)


+(D)


+ Hypsarrhythmia


65


Metachromatic leukodystrophy


+/- (D)



66


Adrenoleukodystrophy


+ (D)



67


Zellweger’s syndrome


+ (D)


+ Spk


68


MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke)


+(D)


+(F) Spk, PLEDs


69


MERRF syndrome (myoclonus with epilepsy and ragged red fibers)


+/- (D)


+ (D)


70


PKU (phenylketonuria)


+ (D)


+ (D) Hypsarrhythmia


71,72


Batten’s disease (neuronal ceroid lipofuscinosis)


++ (D)


++ (D) Spk by low-frequency photic stimulation (see Fig. 9-11)


73,74


Hallervorden-Spatz disease


+ (D)


+ (F, D) Delta/theta/Spk


75


Infantile neuroaxonal dystrophy (Seitelberger’s disease)


Fast activity


+/- (D) Theta, delta


76,77


Wilson’s disease (hepatolenticular degenerative disease)


+ (D)


+/- (D) Delta/theta/sharp waves


78


Menke’s disease (kinky-hair disease)


+ (D)


+ (F) Spk, hypsarrhythmia


79


Tourette syndrome


+/- (D)


+/- (D, F) Central Spk


80


Lafora disease


+ (D)


++ (D, F) Spk, photoparoxysmal response, myoclonus


81


Baltic myoclonic epilepsy (Unverricht-Lundborg type)


+ (D)


++ (D) Photoparoxysmal response


82


Alper’s disease


+/-


++ (F, D)


83


Tuberous sclerosis


+ (D, F)


++ (F, D) Hypsarrhythmia


84,85


Sturge-Weber syndrome


+ (F)


+ (F) Spk, hypsarrhythmia


86


Down’s syndrome


+/-


+/-


87


Hereditary optic nerve atrophy (Leber’s disease)


+/-



88


Myotonic dystrophy


+ (D)



89


Congenital muscular dystrophy (Fukuyama type)


+ (D)


+ (D)


90


Angelman syndrome (happy puppet syndrome)


++ (D)


+ (D) Spk


91


Rett syndrome


+ (D)


++ (F) Spk, central Spk, Lennox-Gastaut syndrome (slows Spk wave)


92,93


V. Inflammatory/Infectious Disease





Acute purulent meningitis


++ (D)


+ (D)


94


Infectious mononucleosis


+ (D)


+/- (D)


95


Aseptic meningitis


+/-



96


Encephalitis


++ (D)


+ (D)


94


Herpes encephalitis


++ (F)


++ (F) PLEDs (see Figs. 10-39 and 10-41A and B)


96


Rasmussen’s encephalitis


+ (F)


++ (F)


97


Congenital rubella encephalitis


++ (D)


+ (D)


98


Progressive rubella panencephalitis


+ (D)


+ (D) Periodic discharges, myoclonus


99


Congenital cytomegalovirus disease


+ (D, F)



100


West Nile virus


+ (D)



101


Rabies


+ (D)



96


Rickettsial infections


+ (D, F)


+ (D, F)


96


Lyme disease


+ (D)



102


Fungal disease


+ (D, F)



96


AIDS (acquired immunodeficiency syndrome)


+ (D, F)


+ (D)


103


Cysticercosis


+ (D, F)


+ (F)


96


Echinococcosis


+ (D, F)


+ (D)


96


Toxoplasmosis


+ (D)


+ (D) Hypsarrhythmia


96,100


African trypanosomiasis (sleeping sickness)


+ (D)


+ (D)


96


Malaria


+ (D)


+/-


96


Sydenham’s chorea


+(D)


+/-


94


Neuro-Behçet’s disease (uveomeningitis)


+(D)


+(D)


99


Neurosyphilis


+(D, F)


+(F)


94,96


Hemiconvulsions, hemiplegia, and epilepsy (HHE syndrome)


+(F)


+(F) Spk, SW


104


Brain abscess


++(F/D)


+(F,D) PLEDs


105,106


VI. Dementia





Alzheimer’s disease


+(D)


+/- Triphasic


107-109


Pick’s disease (frontotemporal dementia)




110


Parkinson’s disease


+(D)



111


Progressive supranuclear palsy


+/-(D)


+ FIRDA (frontally predominant RDA*)


112


Dementia with Lewy bodies


+ (D)


+ FIRDA (frontally predominant RDA*)


113,114


Huntington’s chorea


+/- low voltage



115,116


Normal pressure hydrocephalus


+/- (D)


+ (D) Slow-wave bursts


117


Depression




118


Creutzfeldt-Jakob disease


++ (D)


++ (D) Periodic triphasic waves (see Fig. 10-32A-D)


119,120


VII. Others





Multiple sclerosis


+/- (D, F)


+/- (D, F)


94


Reye’s syndrome


++ (D)


+14- and 6-Hz positive spikes (see Fig. 11-16)


121,122


Subacute sclerosing panencephalitis (SSPE)


+


++ (D) Periodic burst (see Fig. 10-31A and B)


96,123


++, prominent, frequent, high incidence; +, often present; +/-, may or may not be present or low incidence; -, most often not present or none; D, diffuse; F, focal; Spk, spike or spike wave; SW, spike and wave; FIRDA, frontal intermittent rhythmic delta activity; PLEDs, periodic lateralized epileptiform discharges; ↑, increase.

Only gold members can continue reading. Log In or Register to continue

Nov 14, 2018 | Posted by in NEUROLOGY | Comments Off on Diffuse EEG Abnormalities
Premium Wordpress Themes by UFO Themes