5th Edition

The EEG in Cerebral Inflammatory Processes
Barbara F. Westmoreland
The electroencephalogram (EEG) in meningitis shows various degrees of slow-wave abnormalities, depending on the type of meningitis and the degree of involvement of the central nervous system (CNS).
Moderate to severe diffuse slow-wave abnormalities are often present in acute purulent meningitis, and paroxysmal epileptiform activity may be present in those patients who have seizures (Kooi et al., 1978).
The electroencephalographic findings in tuberculous meningitis vary according to the location of the inflammatory process. In basal meningitis, the EEG may be normal and show only mild nonspecific slowing. When the inflammatory process involves the cortical meninges, moderate to severe slowing occurs (Fig. 16.1), depending on the degree of cortical involvement, the rate of progression of the disease process, the level of consciousness, the presence of metabolic or systemic factors, the pulmonary state of the patient, and the effects of medication (Radermecker, 1977). As with purulent meningitis, more severe slow-wave abnormalities are present in children, often with maximal slowing over the posterior head regions (Kiloh et al., 1972).
In aseptic meningitis, the EEG may be normal or show only mild slowing, and the EEG usually returns to normal within 1 to 2 weeks (Radermecker, 1977). The electroencephalographic findings may not necessarily correlate with the clinical severity of the inflammatory process or the development or degree of postinfectious sequelae (Radermecker, 1977).
Patients in whom meningoencephalitis develops in association with infectious mononucleosis may have mild to moderate, diffuse, or focal slow-wave abnormalities that may or may not coincide with the area of maximal neurological dysfunction (Schnell et al., 1966). On occasion, focal epileptiform abnormalities and, rarely, periodic slow-wave complexes have been observed in patients who experience seizures (Greenberg et al., 1982; Radermecker, 1977; Schnell et al., 1966).
The rate and degree of the improvement in the electroencephalographic abnormalities after treatment have some diagnostic and prognostic value (Radermecker, 1977). One of the characteristic features of meningococcal meningitis is the rapid improvement in the electroencephalographic findings, with the findings often returning to normal within 1 or 2 weeks after treatment (Turrell and Roseman, 1955). In other types of purulent meningitis and tuberculous meningitis, the electroencephalographic abnormalities often require several weeks to resolve (Kiloh et al., 1972; Kooi et al., 1978).
The EEG usually returns to normal in patients with uncomplicated meningitis (Kooi et al., 1978); however, persistent electroencephalographic abnormalities or evidence of deterioration in the EEG suggests an unfavorable course, the development of a complication such as an abscess or hydrocephalus, or the presence of residual brain damage (Kooi et al., 1978; Radermecker, 1977). Although the electroencephalographic findings are not essential for making the specific diagnosis of meningitis, the EEG and particularly serial recordings are helpful in following the course of the disease, detecting the development of complications or relapse, and indicating the presence of sequelae or residual brain damage (Radermecker, 1977) (Table 16.1).
The electroencephalographic findings in encephalitis are similar to those in meningitis, although the abnormalities often are more severe; this may be a helpful point in the differential diagnosis.
The EEG is almost always abnormal during the acute phase of encephalitis (Kooi et al., 1978), with the most frequent finding being the presence of diffuse high-voltage, arrhythmic, and/or rhythmic delta slowing (Fig. 16.2, top). Diffuse polymorphic arrhythmic delta activity is more likely to occur when the white matter is involved, whereas paroxysmal, bisynchronous slow-wave activity is more likely to be present when the disease process involves the subcortical gray matter (Gloor et al., 1968). The degree of slowing depends on the severity of the infection, the amount of cerebral involvement, the level of consciousness, and other associated systemic or metabolic factors (Cobb, 1975; Kiloh et al., 1972; Scott, 1976). In general, the leukoencephalitides, which primarily involve the white matter and which are caused by the group B nonneurotropic viruses (measles, rubella, and variola) and the postvaccinal states, are associated with more severe electroencephalographic abnormalities than are those caused by the group A neurotropic viruses (mumps, St. Louis, and equine encephalitis with the exception of the severe Eastern form) (Gibbs et al., 1964; Kiloh et al., 1972). Children often show more severe electroencephalographic abnormalities than do adults. Epileptiform abnormalities also may be present, particularly if the patient is having seizures (Fig. 16.2, bottom).
Slow-wave abnormalities have also been observed during the acute stages of uncomplicated childhood infections, such as measles, mumps, rubella, chickenpox, and scarlet fever (Gibbs et al., 1959), in which there is no overt evidence of

nervous system involvement. The electroencephalographic abnormalities occur most frequently with measles infection (Gibbs et al., 1959), in which moderate to severe slow-wave abnormalities may be present as early as 1 to 4 days before the rash appears, reaching a maximum on the first day of the rash and then subsiding during the next 8 to 10 days (Pampiglione, 1964b). Transient slow-wave abnormalities also have been observed over the posterior head regions after measles vaccination (Pampiglione et al., 1971).
Figure 16.1. EEG showing generalized slowing in an 11-month-old boy with tuberculous meningitis.
The electroencephalographic abnormalities usually diminish in association with clinical improvement, but on occasion the electroencephalographic changes lag behind the clinical findings. However, persistent or increased abnormalities, particularly if they are focal, are associated with an increased likelihood of brain damage or postencephalitic epilepsy. A return to a normal electroencephalographic pattern does not preclude residual brain damage (Kooi et al., 1978).
Congenital rubella encephalitis is associated with seizures and congenital malformations. The EEG abnormalities, which are usually apparent during the first month of life, consist of high-voltage slow waves and sharp-wave transients. The greatest percentage of abnormalities occur in patients who ultimately die or who have cataracts (Desmond et al., 1967; Dreyfus-Brisac and Ellingson, 1972). A lower incidence of abnormal EEGs is seen in patients with a hearing loss (Desmond et al., 1967).
Progressive rubella panencephalitis is an entity that consists of a delayed progressive neurological deterioration that occurs in the second decade of life in children who had congenital rubella (Vinken and Bruyn, 1978a; Wolinsky et al., 1976). The pathological findings are those of a subacute or chronic progressive panencephalitis. The EEG shows generalized slowing with intermittent slow waves. Periodic multiple spike complexes associated with myoclonic movements have been seen (Vinken and Bruyn, 1978a). Periodic high-voltage slow-wave complexes, occurring every 5 to 8 seconds and having features similar to those seen in subacute sclerosing panencephalitis, have also been seen but are not a constant finding (Vinken and Bruyn, 1978a; Wolinsky et al., 1976).
Figure 16.2. EEG of 2½-year-old boy with encephalitis. Top, generalized polymorphic delta activity; bottom, recorded seizure activity consisting of repetitive sharp waves over the left parietal and occipital head regions.
Congenital cytomegalovirus disease can cause severe damage to the developing CNS of fetuses and infants, resulting in various types of congenital defects, mental and motor retardation, and seizures (Dreyfus-Brisac and Ellingson, 1972). The EEG often shows significant abnormalities consisting of focal or generalized epileptiform discharges and diffuse or focal slow-wave abnormalities. Hypsarrhythmia, associated with infantile spasms, can also be seen (Dreyfus-Brisac and Ellingson, 1972). Cytomegalovirus disease can also occur in immunosuppressed patients, transplant recipients, and patients with AIDS; the EEG may show diffuse or focal abnormalities, depending on the involvement of the CNS.
The enteroencephalitides caused by coxsackievirus and enterocytopathogenic human orphan (ECHO) virus, which predominantly affect infants and young children, are accompanied by varying degrees of diffuse slow-wave abnormalities in the EEG (Radermecker, 1977).
Arthropod-borne viral encephalitides may be associated with changes in the EEG. In the mosquito-borne encephalitides, which include Western equine, Eastern equine, St. Louis, and Japanese encephalitis, variable slow-wave abnormalities


can be seen in the EEG, which may or may not show a correlation with the clinical picture (Radermecker, 1977). Diffuse slow-wave abnormalities with at times more focal features and epileptiform activity may be seen in California encephalitis, and there is a fairly good correlation between the EEG and clinical findings, both during the acute stages of the disease and on follow-up examinations (Grabow et al., 1969; Radermecker, 1977).
Table 16.1. EEG Abnormalities in Inflammatory Conditions
Condition EEG Findings
   Acute purulent meningitis Moderate to severe diffuse slow-wave abnormalities
   Tuberculous meningitis Mild to moderate slowing
   Aseptic meningitis Normal or mild slowing
   Infectious mononucleosis Mild to moderate slow-wave abnormalities; rarely epileptiform abnormalities
   Acute encephalitis Mild to severe slow-wave abnormalities; epileptiform abnormalities may also be present
   Congenital rubella encephalitis High-voltage slow waves and sharp waves
   Progressive rubella encephalitis Generalized slowing; on occasion spike discharges; rarely periodic slow-wave complexes
   Congenital cytomegalovirus disease Diffuse and focal slow-wave abnormalities; focal and generalized epileptiform abnormalities
   California encephalitis Varying degrees of diffuse slow-wave abnormalities
   Coxsackie encephalitis Varying degrees of diffuse slow-wave abnormalities
   ECHO encephalitis Varying degrees of diffuse slow-wave abnormalities
   Western equine encephalitis Varying degrees of diffuse slow-wave abnormalities
   Eastern equine encephalitis Varying degrees of diffuse slow-wave abnormalities
   St. Louis encephalitis Varying degrees of diffuse slow-wave abnormalities
   Japanese encephalitis Varying degrees of diffuse slow-wave abnormalities
   West Nile encephalitis Varying degrees of diffuse slow wave abnormalities
   Tick-borne encephalitis Varying degrees of diffuse slow-wave abnormalities
   Rasmussen-Aguilar syndrome Focal and generalized epileptiform abnormalities that migrate to different areas of the brain
   Herpes simplex encephalitis Periodic lateralized epileptiform discharges
   Rabies Widespread slowing
Rickettsial diseases
   Typhus Diffuse or focal slow-wave abnormalities
   Rocky Mountain spotted fever Diffuse or focal slow-wave abnormalities
   Tsutsugamushi fever Diffuse or focal slow-wave abnormalities
Fungal diseases
   Histoplasmosis Diffuse slow-wave abnormalities
   Blastomycosis Diffuse slow-wave abnormalities
   Coccidioidomycosis Diffuse slow-wave abnormalities
   Cryptococcosis Diffuse slow-wave abnormalities
   Aspergillosis Focal slow-wave abnormalities
   Nocardiosis Focal slow-wave abnormalities
   Mucormycosis Focal slow-wave abnormalities
   Candidiasis Focal slow-wave abnormalities
Prion diseases
   Creutzfeldt-Jakob disease Generalized periodic sharp waves
   Kuru Slowing of the background
   Subacute sclerosing panencephalitis Generalized stereotyped periodic slow-wave complexes
   Cysticercosis Focal epileptiform and focal and generalized slow-wave abnormalities
   Echinococcosis Focal delta slowing and generalized slow-wave abnormalities
   Toxoplasmosis Infants: focal epileptiform abnormalities, hypsarrhythmia, delta slowing asymmetry
Adults: normal or focal or generalized slow-wave abnormalities
   African trypanosomiasis Intermittent slow-wave bursts; abnormal sleep patterns
   Malaria Focal and generalized slowing
   Filariasis Normal or diffuse slow-wave abnormalities
   Trichinosis Diffuse slowing
Miscellaneous conditions
   Sydenham’s chorea Mild to moderate generalized slow-wave abnormalities; rhythmic slowing over posterior head regions
   Reye’s syndrome Moderate to severe slow-wave abnormalities; epileptiform activity and seizure discharges
   Neurosyphilis Mild to moderate slowing
   Neuro-Behçet’s disease Paroxysmal slow waves and generalized delta slowing
   Multiple sclerosis Normal or diffuse or focal slow-wave abnormalities
   Hemiconvulsions, hemiplegia, epilepsy (HHE) syndrome Unilateral epileptiform abnormalities and suppression of activity over affected hemisphere
The EEG in patients with meningitis and/or encephalitis secondary to West Nile virus has been described as showing generalized slowing that may be maximal over the frontal or temporal regions (Klein et al., 2002).
In tick-borne encephalitis, which includes Russian summer-spring encephalitis, Colorado tick fever, and the tick-borne encephalitis seen in Central and Eastern Europe, Scandinavia, and Finland, slow-wave abnormalities may be present prior to the onset of symptoms. The abnormalities do not necessarily correspond with the clinical symptoms and severity of the infection; slow-wave abnormalities, however, may continue to be present in those patients with postencephalitic symptoms and in some patients after the disease appears to have resolved (Hanzel, 1961; Lehtinen and Halonen, 1984; Radermecker, 1977).
EEG recordings have been done only rarely in patients with rabies. The recordings have been described as showing a depression or “extreme desynchronization” in one case and nonspecific findings in two other cases (Gastaut and Miletto, 1955; Radermecker, 1977). Prominent slowing with maximum over the vertex was noted in a case observed by Zschocke (1987). Diffuse slow-wave abnormalities similar to those seen in other postvaccinal states may be present after rabies vaccination (Radermecker, 1977).
Although abnormalities are usually not seen with pure spinal cord poliomyelitis, EEG abnormalities have been seen in polio, indicating a subclinical cerebral involvement (Radermecker, 1977).
The EEG recordings in the rickettsial infections (Eurasian typhus or spotted fever, Rocky Mountain spotted fever, and tsutsugamushi fever) range from normal to those showing diffuse or focal slow-wave abnormalities, with epileptiform activity present in those patients who develop seizures (Radermecker, 1977). The degree of EEG abnormality usually reflects the degree of encephalitic involvement.
Lyme disease, which is caused by a spirochete and is transmitted by a tick, may be accompanied by neurological symptoms and signs, including meningoencephalitis, cranial neuritis, and a radiculoneuritis (Pachner and Steere, 1985). Mild slowing has been seen in patients with encephalitic symptoms, and this has also been seen in some patients without evidence of encephalitis (Pachner and Steere, 1985).
Encephalitis or meningitis caused by fungal diseases (histoplasmosis, blastomycosis, coccidioidomycosis, and cryptococcosis) is associated with diffuse slow-wave abnormalities. These changes are similar to those produced by bacterial and viral agents. More focal EEG abnormalities may be present with focal cerebral involvement secondary to mycotic abscesses, granulomata, ischemia, vasculitis, thrombosis, hemorrhage, embolization, necrosis, or demyelination; these can be seen with aspergillus, nocardiosis, mucormycosis, and candidiasis (Radermecker, 1977). These complications are particularly likely to occur in compromised patients with altered immune states (Vinken and Bruyn, 1978b). As fungal infections tend to recur, the EEG may be helpful in following the clinical course of the patient and calling attention to a possible recurrence of the infection or the development of complications (Radermecker, 1977). The EEG may also be useful in monitoring the therapeutic and toxic effects of drugs (Radermecker, 1977).
As a rule, most of the different types of encephalitis do not give rise to specific types of EEG patterns. Instead, the EEG abnormalities are most often expressed as diffuse or focal slow-wave abnormalities, with the degree and extent of the slowing reflecting the intensity of parenchymal involvement (Radermecker, 1977).
Rasmussen’s Encephalitis
Rasmussen’s encephalitis is a chronic devastating disease occurring in children and young adults that predominantly affects one hemisphere and is characterized by progressive neurological and intellectual deterioration, hemiparesis, and recurrent episodes of intractable seizures (Aguilar and Rasmussen, 1960; Rasmussen and McCann, 1968). The seizures are variable; one type of seizure may be present at one time to be replaced by a different type of seizure occurring in a different location at another stage of the disease process. Epilepsia partialis continua is commonly seen in this entity (Andermann, 1991). The EEG shows various types of epileptiform and slow-wave abnormalities. The epileptiform abnormalities consist of focal, multifocal, unilateral, or bilaterally synchronous discharges (Andermann, 1991; Andrews, 1997), which can migrate or spread to different areas of the brain during the disease process (Fig. 16.3). Initially, the epileptiform activity is more prominent over the involved hemisphere. Later there is the development of bilateral epileptiform activity. As the disease progresses, the epileptiform activity becomes more frequent over the contralateral hemisphere and less frequent over the involved hemisphere (Andrews, 1977).
The pathological changes are consistent with a chronic encephalitis with perivascular inflammation, astrocytosis, lymphocytosis, gliosis, neuronal loss, and atrophy of the involved cerebral hemisphere (Andermann, 1991). There are areas of an active inflammatory process in some regions of the brain, while other regions show scarring or evidence of a “burned out” encephalitis (Rasmussen and McCann, 1968), which suggests that this may represent a chronic smoldering process that flares up intermittently, with an exacerbation of seizures and neurological and mental deficit (Andermann, 1991).
Investigators have reported the presence of an antibody to the GluR3 protein of the glutamate receptor in a subgroup of patients with Rasmussen’s encephalitis and that rabbits immunized with the GluR3 antibody developed a syndrome similar to Rasmussen’s encephalitis, which would suggest an immunopathological etiology (Andrews, 1996; Rogers, 1994).
There has also been a report of a cytomegalovirus genome found in some patients with Rasmussen’s encephalitis, and the authors have suggested that the disease process could be

related to the persistence of the virus in the CNS (Jay et al., 1995; Power et al., 1990).
Figure 16.3. Serial EEG samples showing various types of electroencephalographic abnormalities in a patient with Rasmussen encephalitis; upper left segment shows generalized paroxysmal slow-wave abnormalities; upper middle shows focal spikes over the left posterior head region; upper right shows sharp waves over the left hemisphere; lower left shows rhythmic slowing and focal spikes in the right central-parietal derivation; lower middle shows spike and wave discharges maximal over the right hemisphere; lower right shows status epilepticus with repetitive generalized spike discharges, occurring maximally over the anterior head regions.
These findings suggest that Rasmussen’s encephalitis is a chronic smoldering process that may be secondary to ongoing viral and/or immunological activity with an intermittent exacerbation of seizures and progressive neurological and mental deficit.
The interest in the possibility that immune mediated mechanisms may play a role in Rasmussen’s encephalitis has led to a trial of immunosuppressive therapy, and there is a report in which the EEG findings, seizures, and clinical picture transiently improved in a few patients following plasmapheresis (Andrews, 1996). The EEG thus can be a helpful adjunct in following the course of patients undergoing various forms of therapy.
Herpes Simplex Encephalitis
The EEG often shows a characteristic pattern and temporal evolution (Kiloh et al., 1972) that can be of great value in making the diagnosis of herpes simplex encephalitis, especially when serial recordings are obtained (Upton and Gumpert, 1970). During the earlier stages of the disease process, the background activity is disorganized, and polymorphic delta activity develops in a focal or lateralized fashion, with a predominance over the involved temporal region; soon after this, focal or lateralized sharp- or slow-wave complexes appear, usually having a maximal expression over the involved temporal region (Ch’ien et al., 1977; Cobb, 1975; Gupta and Seth, 1973; Illis and Taylor, 1972; Kiloh et al., 1972; Radermecker, 1977; Rawls et al., 1966). These complexes rapidly evolve into a periodic pattern, with the sharp waves having a stereotyped appearance and recurring every 1 to 3 seconds (Fig. 16.4, top). The periodic pattern is usually seen between 2 and 5 days after the onset of the illness (Upton and Gumpert, 1970) but, on occasion, it has been observed up to 24 and 30 days after the onset of the illness (Elian, 1975; Illis and Taylor, 1972). If there is a bilateral involvement of the brain, bilateral periodic complexes may be present (Fig. 16.4, bottom), occurring synchronously or independently over the two hemispheres but often having a time-locked relationship with one another (Gaches and Arfel, 1972; Gupta and Seth, 1973; Illis and Taylor, 1972; Smith et al., 1975). Focal or lateralized electrographic seizure discharges,

consisting of repetitive sharp or slow waves or spike or polyspike bursts, may be present over the involved area or hemisphere. During this time, there is a transient obliteration of the periodic discharges on the side of the seizure discharges (Gaches and Arfel, 1972; Gupta and Seth, 1973; Smith et al., 1975). In the later stages of a fatal herpes simplex infection, the electrographic seizure discharges may occur in association with the periodic discharges without altering them. Additionally, during the later stages of the disease process, the periodic complexes often have a broader slow-wave appearance and a longer interburst interval. During the final stages of a fatal infection, the EEG assumes an almost isoelectric appearance.
Figure 16.4. EEG of 68-year-old man with herpes simplex encephalitis. Top, periodic sharp waves over the left hemisphere; bottom, development of bilateral periodic complexes.
In nonfatal herpes simplex encephalitis, the periodic complexes disappear as the disease process resolves; they are replaced by focal or lateralized slow-wave abnormalities or attenuation of activity over the involved area (Cobb, 1975; Kiloh et al., 1972). The resolution of the electroencephalographic abnormalities often lags behind the improvement in the clinical state (Illis and Taylor, 1972); the EEG frequently continues to show residual slow-wave abnormalities and focal epileptiform activity over the involved area.
As in adults, the presence of periodic complexes is a prominent feature in infants with herpes simplex encephalitis (Mizrahi and Tharp, 1982; Pettay et al., 1972; Sainio et al., 1983) (Fig. 16.5). The periodic activity consists of slow- or sharp-wave complexes that may occur in a focal or multifocal fashion or have a shifting emphasis from area to area (Mizrahi and Tharp, 1982; Pettay et al., 1972). The periodic waveforms are usually stereotyped in the same patient but vary from patient to patient in morphological appearance. The periodic discharges may occur as intermittent paroxysms or persist throughout the recording without being altered by focal seizure discharges in other locations (Mizrahi and Tharp, 1982; Sainio et al., 1983). In the infants who survive, subsequent EEGs continue to show the presence of focal or multifocal epileptiform abnormalities and/or localized areas of attenuation overlying cystic areas of the brain (Smith et al., 1977). In infants who ultimately die, serial EEG recordings show a progression to a low-voltage or isoelectric tracing (Mizrahi and Tharp, 1982).
Figure 16.5. EEG of 2-week-old infant with neonatal herpes simplex encephalitis showing periodic discharges over the left hemisphere.
Although the findings in herpes simplex encephalitis are not pathognomonic for the disease, the presence of unilateral or bilateral periodic complexes in association with a febrile illness and a rapid evolution of neurological signs are strongly suggestive of herpes simplex encephalitis (Smith et al., 1975).
Acquired Immune Deficiency Syndrome (AIDS)
The human immunodeficiency virus (HIV) is a neurotropic virus involving both the nervous system and the immune system (Enzensberger et al., 1986; Klatzman et al., 1984; Levy and Bredesen, 1988; Nicholson, 1986). The most common CNS involvement consists of subacute encephalitis with dementia, also referred to as AIDS encephalopathy or the AIDS dementia complex (Levy and Bredesen, 1988; Snider et al., 1983). Various types of EEG abnormalities can be seen in patients with AIDS, including focal or generalized slowing, asymmetries, paroxysmal abnormalities, and/or epileptiform abnormalities (Bernad, 1991; Tinuper et al., 1990). These findings can occur as a result of primary infection by the AIDS virus or as a result of various opportunistic infections (candidiasis, cryptococcosis, toxoplasmosis, cytomegalovirus), neoplasms (primary CNS lymphoma, Kaposi’s sarcoma), cerebrovascular complications, and/or the superimposed effects of more widespread systemic involvement (Levy and Bredesen, 1988).

Prion Diseases
Creutzfeldt-Jakob Disease
Creutzfeldt-Jakob disease is one of the prion diseases causing a diffuse disorder of the CNS that is now believed to be due to abnormal isoforms of the prion protein. The disease is characterized by progressive dementia, motor dysfunction, myoclonus, and a characteristic periodic electroencephalographic pattern that is valuable in making or confirming the diagnosis (Kiloh et al., 1972; May, 1968; Nevin et al., 1960).
The earliest electroencephalographic changes consist of a disorganization and decrease of normal background activity and the development of progressive slow-wave abnormalities (Burger et al., 1972). The slow-wave abnormalities are usually generalized, but at times they occur in a more focal or lateralized fashion. As the disease progresses, diphasic or triphasic slow-wave discharges appear. Initially, these discharges occur in a sporadic or intermittent fashion and may be asymmetric or predominate over one region (Burger et al., 1972), but eventually they evolve into the characteristic pattern, consisting of generalized and bisynchronous continuous periodic stereotyped sharp waves, recurring at intervals of 0.5 to 1 second and having a duration of 200 to 400 msec (Fig. 16.6) (Gloor, 1980; Jones and Nevin, 1954; Kiloh et al., 1972; May, 1968; Nevin et al., 1960; Radermecker, 1977). A majority of patients with Creutzfeldt-Jakob disease develops the characteristic EEG pattern by 12 weeks of the disease process (Levy, 1986). On a few occasions the discharges appear as periodic lateralized epileptiform discharges (PLEDs) before evolving into a bilateral pattern (Au et al., 1980). Myoclonic jerks often occur in association with the periodic sharp waves; however, there is not always a constant relationship between the myoclonic jerks and periodic sharp waves; one can occur without the other (Radermecker, 1977). This is particularly true during sleep or late in the course of the disease, when the myoclonic jerks decrease or disappear, but the periodic sharp waves persist (Burger et al., 1972; Jones and Nevin, 1954).
Figure 16.6. Typical EEG pattern of continuous bilaterally synchronous periodic sharp waves in 55-year-old woman with Creutzfeldt-Jakob disease.
One characteristic feature of the periodic discharges in Creutzfeldt-Jakob disease is the reactivity of the sharp waves to alerting or afferent stimuli (Radermecker, 1977). Prior to the time when the periodic pattern has been established or when the sharp waves occur in a more intermittent or sporadic fashion, alerting the patient or arousing the patient out of sleep may bring out the periodic pattern (Cobb, 1975; F. W. Sharbrough, personal communication). When the periodic pattern is present, rhythmic photic, auditory, or somatosensory stimuli can pace or set the rhythm of the sharp waves if the frequency of the stimuli falls near the range of the frequency of the spontaneous periodic pattern. However, loud noises and certain types of drugs, such as diazepam and the barbiturates, can temporarily abolish the periodic sharp waves and myoclonic jerks (Elliott et al., 1974; Jones and Nevin, 1954; Nelson and Leffman, 1963; Radermecker, 1977).
As the disease progresses, the interburst interval increases and the amplitude of the periodic sharp waves decreases. In the final stages of the disease, the EEG becomes almost isoelectric, with intermittent bursts of sharp or slow waveforms that finally disappear in the terminal stages of the disease (Nevin et al., 1960).
In Heidenhain’s variant of the disease, where there is a predominant involvement of the occipital head regions, the EEG often shows more focal abnormalities consisting of slowing and periodic complexes over the posterior head regions (Furlan et al., 1981). Some lateralization of the abnormalities may occur in the early stages, but the abnormalities usually become bilateral as the disease progresses. The periodic complexes may remain confined to the posterior head regions throughout the disease (Furlan et al., 1981), or they may become more widespread with a maximal amplitude over the posterior head regions.
On occasion Creutzfeldt-Jakob disease may progress rapidly, and the typical EEG abnormalities may evolve over a period of 1 to 3 weeks, and serial EEGs are helpful in making or confirming the diagnosis (Drury and Beydou, 1996; Levy et al., 1986). One should be aware, however, that some patients with Creutzfeldt-Jakob disease may not show the typical pattern of periodic sharp waves (Brown et al., 1984; Drury and Beydou, 1996; Tietjen and Drury, 1990).
The “mad cow” variant of Creutzfeldt-Jakob disease has been described as occurring at a younger age of onset than is typical for Creutzfeldt-Jakob disease and without the typical EEG changes of Creutzfeldt-Jakob disease (Will et al., 1996). The other atypical variants of Creutzfeldt-Jakob disease don’t usually show the typical pattern of the generalized periodic sharp waves (Zerr et al., 2000).
Although the electroencephalographic findings are not pathognomonic for Creutzfeldt-Jakob disease, the presence of the periodic electroencephalographic pattern in association with the clinical findings of progressive dementia and myoclonus in an adult is a strong indication of Creutzfeldt-Jakob disease.
Kuru is a fatal cerebellar degenerative disease seen in the Fore people of New Guinea described by Gajdusek and Zigas (1957) and is now considered one of the variants of

prion disease. Although the disease primarily involves the cerebellum, cerebral involvement occurs in the late stages as manifested by dementia and loss of emotional control. The EEG findings consist of slowing the alpha rhythm, an increase in theta activity, and, on occasion, delta slowing (Cobb et al., 1973). There has been no evidence for periodic or repetitive complexes (Cobb et al., 1973).
Subacute Sclerosing Panencephalitis
Subacute sclerosing panencephalitis (SSPE) is an inflammatory disease that occurs in children and adolescents; it is believed to be caused by the measles virus and is characterized by abnormal movements, a progressive intellectual deterioration, and a diagnostic electroencephalographic pattern. The characteristic electroencephalographic pattern was first described by Radermecker (1949) and Cobb and Hill (1950) and consists of high-voltage (300–1,500 mV) repetitive polyphasic and sharp- and slow-wave complexes ranging from 0.5 to 2 seconds in duration, usually recurring every 4 to 15 seconds (Cobb, 1966) (Fig. 16.7). On rare occasions, these complexes may occur at intervals ranging up to 1 to 5 minutes (Reiher et al., 1973; Westmoreland et al., 1977).
The periodic complexes may be present at any stage of the disease, but they usually are seen during the intermediate stages. Although the form and appearance of the periodic complexes are fairly constant and stereotyped in a single recording, the shape of the complexes varies in different patients and can change in the same patient at different stages of the disease process (Cobb, 1966; Kiloh et al., 1972). The complexes are usually generalized and bisynchronous, but at times they may be asymmetric, have a time lag from side to side or front to back (Cobb, 1966; Kooi et al., 1978), or occur in a more lateralized or focal fashion, particularly in the earlier stages of the disease. Initially, the complexes may occur at irregular intervals, but, once established, the complexes recur at regular intervals, although the repetition rate may vary during the course of the disease (Cobb, 1966; Kiloh et al., 1972). Afferent stimuli do not usually affect the periodic complexes (Cobb, 1966; Radermecker, 1977); however, on rare occasions, the complexes can be evoked by external stimuli (Cobb, 1966; Westmoreland et al., 1979). This occurs when the complexes are present in an inconstant manner, either when they first make their appearance or toward the end of the period of remission (Cobb, 1966; Radermecker and Poser, 1960). Once the regular pattern of the complexes has been established, however, the complexes are no longer influenced by external stimuli (Radermecker and Poser, 1960). Drugs usually have little effect on the periodic complexes (Radermecker, 1977), although one report described the occurrence of periodic patterns after an intravenous injection of diazepam (Lombroso, 1968).
Figure 16.7. Typical EEG pattern of periodic complexes in 11-year-old girl with subacute sclerosing panencephalitis (SSPE) (run at slow paper speed).
A prominent feature of SSPE is the stereotyped motor jerks or spasms occurring with the periodic complexes. The movements are often described as myoclonic jerks; however, they do not have the momentary lightning-quick nature of true myoclonus; instead, the movements consist of an initial “shock-like abruptness,” followed by a momentary arrest of the movement, and then a gradual melting away to the position of rest (Metz et al., 1964). On less frequent occasions, the periodic complexes may be associated with an inhibitory phenomenon such as an arrest of movement, loss of tone, or drop attacks (Pampiglione, 1964a). The abnormal movements usually become evident at about the same time that the periodic complexes appear on the EEG; however, on occasion, and particularly in the early stages of the disease, the periodic complexes may be present without the associated motor movements (Cobb, 1966; Markand and Panszi, 1975). On the other hand, the presence of the motor jerks in the absence of the periodic complexes is uncommon (Cobb, 1966, 1975). The motor movements often disappear during sleep, despite a persistence of the periodic complexes. Certain drugs, such as diazepam, may reduce or abolish the motor movements without altering the electroencephalographic complexes.
The resting EEG may be relatively normal when the complexes first appear (Cobb, 1966; Kiloh et al., 1972). As

the disease evolves, however, the EEG shows various changes consisting of slowing and disorganization of the background, asymmetry of the background activity, or both. These changes are followed by an increase in the slow-wave abnormalities, usually occurring in a diffuse manner but at times having a focal or lateralized emphasis and coinciding with the area of maximal neurological involvement (Cobb, 1966; Radermecker, 1977). In the later stages of the disease, polymorphic delta activity or intermittent frontal dominant monorhythmic slow-wave activity may be present (Markand and Panszi, 1975). On occasion, there may be a transient flattening or attenuation of activity after the periodic complexes (Markand and Panszi, 1975; Radermecker, 1977). Various types of epileptiform discharges, spikes, sharp waves, or spike-and-wave complexes occurring in a focal or generalized fashion also may be present (Cobb, 1966; Markand and Panszi, 1975). Patients who have a remission or an improvement in the clinical state show a corresponding improvement on the EEG (Markand and Panszi, 1975).
The typical stages of sleep become less recognizable as the disease progresses, and identifiable sleep stages become limited to two main types: a low-voltage fast pattern with or without spindle activity and a high-voltage slow-wave pattern (Kooi et al., 1978; Radermecker, 1977). In the later stages of the disease, sleep spindles, V waves, and K complexes disappear and the electroencephalographic differentiation of the various stages of sleep is no longer possible (Petre-Quadens et al., 1968). The periodic complexes often persist during sleep, although their shape and frequency may be modified (Cobb, 1966). On rare occasions, periodic complexes may be activated or occur predominantly during the sleep recording (Westmoreland et al., 1977).
As the disease progresses, there may be a shortening in the interval between the complexes (Markand and Parisi, 1975; Wulff, 1982). In the final stages of the disease, there is often a reduction in amplitude and abundance of the electroencephalographic activity, and the recording may become almost isoelectric (Radermecker, 1977). In some instances, however, alpha activity may still be present shortly before death (Cobb, 1966; Markand and Panszi, 1975).
Although other entities may be associated with a periodic pattern, the stereotyped electroencephalographic complexes occurring in a regular and periodic fashion and having a constant relationship to motor movements make this pattern one of the most characteristic and specific of all electroencephalographic patterns (Cobb, 1966, 1975). Close attention to the EEG and clinical features aid in the diagnosis of SSPE and distinguish it from other types of encephalopathies or disease entities (Markand and Panszi, 1975).
Cysticercosis is characterized by multifocal intracranial nodules and calcification secondary to parasitic cysts (Vinken and Bruyn, 1978b). The EEG shows focal epileptiform abnormalities and focal or diffuse slow-wave abnormalities depending on the site of the lesions and the degree of involvement of the brain (Radermecker, 1977; Vinken and Bruyn, 1978b).
Echinococcosis (hydatidosis) may present with cerebral hydatid cysts. More superficial cerebral cysts are associated with focal polymorphic delta slowing, while more deep-seated cysts are associated with unilateral or generalized monomorphic delta activity or paroxysmal slow-wave activity. Epileptiform activity may also be present but is less common (Radermecker, 1977).
Toxoplasmosis may present with focal or multifocal mass lesions, hemorrhagic lesions, metastatic granulomatosis, necrosis, meningoencephalitis, ependymitis, and hydrocephalus (Vinken and Bruyn, 1978b). Congenital toxoplasmosis has a particular affinity for the CNS and can cause severe damage to the fetus, resulting in mental and motor retardation, spasticity, visual difficulties, and seizures. The EEG is usually abnormal in infants with congenital toxoplasmosis and shows a variety of abnormalities consisting of delta slowing, attenuation of background activity, asymmetry, epileptiform abnormalities, and hypsarrhythmia (Dreyfus-Brisac and Ellingson, 1972; Radermecker, 1977).
The acquired form of toxoplasmosis seen in adults does not have the same affinity for the CNS as the congenital form, and the EEG shows less severe abnormalities or may be normal (Radermecker, 1977). Toxoplasmosis, however, is an important opportunistic pathogen in immunocompromised patients, transplant recipients, and patients with AIDS. It commonly involves the CNS, causing focal neurological deficits or a diffuse encephalopathy with corresponding abnormal EEGs.
In African trypanosomiasis (sleeping sickness) there is a disruption of the sleep-wake cycles with patients showing excessive drowsiness and sleepiness and sleep disturbances (Tapie et al., 1996). The waking EEG shows slowing of the background with bisynchronous slow-wave bursts that initially occur at 5- to 15-second intervals (Radermecker, 1977). As the disease progresses, the periodicity becomes more prominent. Later, the alpha activity disappears and the EEG shows a progressive attenuation of the background activity. Epileptiform activity may occur in the late stages of the disease and is often associated with seizures (Radermecker, 1977). Recordings during sleep show significant changes: (a) the various stages of sleep become less distinct as the typical markers of the various sleep stages, such as vertex waves and spindles, disappear, making it difficult to identify the various stages (Radermecker, 1977); (b) there is a telescoping of the various sleep stages; and (c) the more normal sequence of sleep stages is altered. Light sleep is interrupted by frequent arousals. Deep sleep (stage IV) is not always preceded by lighter stages and is also interrupted by frequent arousals. Low-amplitude theta and delta activity ranging from 3 to 7 seconds in duration may occur in a cyclic fashion during stage IV of sleep and may be associated with changes in cardiac and respiratory rhythms and tonic contractions of muscles. The drowsy state of the patient, coupled with the inability to enter sustained levels of deep sleep, produces a state of persistent hypersomnolence, i.e., “a true sleeping sickness” (Radermecker, 1977). With treatment, there is usually a rapid improvement in the EEG (Radermecker, 1977).
In malaria, minor changes may occur in the EEG in the absence of clinical CNS manifestations (Radermecker, 1977).

With cerebral malaria in which the patient is comatose, the EEG shows significant slow-wave abnormalities and, on occasion, spikes and sharp waves. In patients who recover, the EEG usually becomes normal; in patients with sequelae, the EEG may become normal or may continue to show a persistent abnormality (Radermecker, 1977).
In filariasis, the EEG may be normal or mildly abnormal in those patients with neuropsychiatric symptoms, but it is significantly abnormal in those with the encephalitic form (Radermecker, 1977; Vinken and Bruyn, 1978b). On occasion the EEG may become more abnormal when therapy causes lysis of the microfilarie (Radermecker, 1977).
Significant slowing can be seen in the EEG in the acute phase of meningoencephalitis caused by trichinosis; it may be disproportionate to the clinical symptoms. In the chronic phase, the EEG changes are usually less severe than the clinical symptoms (Perot et al., 1963; Radermecker, 1977).
Sydenham’s Chorea
Sydenham’s chorea is a movement disorder that occurs in patients with acute rheumatic fever. Sydenham’s chorea occurs mainly in children and adolescents; it has been reported that more than half of the patients with Sydenham’s chorea have abnormal electroencephalographic findings during the disease process (Johnson et al., 1964; Lavy et al., 1964). The electroencephalographic findings consist of slow-wave abnormalities that vary from a mild slowing of the background to generalized delta slowing, with the degree of slowing being proportional to the severity of the movement disorder (Johnson et al., 1964; Kooi et al., 1978; Usher and Jasper, 1941). The slowing is usually diffuse but often has a maximal expression over the posterior head regions (Fig. 16.8). In addition, brief trains of rhythmic 2- to 3-Hz bilaterally synchronous slow waves may be present over the posterior head regions immediately after eye closure (Johnson et al., 1964). More lateralized slow-wave abnormalities may be present in hemichorea (Kooi et al., 1978). On rare occasions, epileptiform abnormalities have been observed (Johnson et al., 1964). In general, the improvement on the EEG corresponds to the improvement in the clinical state, although on occasion the electroencephalographic abnormalities may lag behind the clinical state (Kooi et al., 1978; Lavy et al., 1964).
Figure 16.8. EEG of 14-year-old boy with Sydenham’s chorea, showing slowing over the posterior head regions.
Figure 16.9. Serial electroencephalograms in 12-year-old girl with Reye’s disease, showing generalized delta slowing (A), low amplitude slowing (B), and suppression of activity (C).
Reye’s Disease
Reye’s disease is a neurological disorder of children and adolescents that is characterized by a rapid, progressive encephalopathy and fatty infiltration of the viscera (Chaves-Carballo et al., 1975). The EEG shows various types of abnormalities that reflect the severity of the clinical state. In

describing the prognostic value of the EEG in Reye’s disease, Aoki and Lombroso (1973) observed that patients whose electroencephalograms showed mild to moderate degrees of theta and delta slowing often survived, whereas patients with severe EEG abnormalities consisting of very low-voltage delta slowing (Fig. 16.9) or a burst suppression pattern usually died. A third group of patients had an intermediate degree of abnormalities consisting of moderate- to high-voltage arrhythmic or semirhythmic delta slowing. Some of those patients survived and some died; serial recordings were helpful in determining whether the patient had a potential for improvement or would progress to an irreversible brain dysfunction.
Triphasic waves, which are seen in hepatic coma and hyperammonemia, are uncommon in Reye’s disease (Aoki and Lombroso, 1973). Epileptiform abnormalities consisting of focal or multifocal sharp-wave discharges and electrographic seizure activity may be present, usually occurring in the later stages of the disease when the patient has deteriorated to a comatose state. It is not uncommon to see lack of clinical-electroencephalographic correlation (that is, seizures without an electroencephalographic abnormality or vice versa) (Aoki and Lombroso, 1973). This is usually a poor prognostic sign.
The electroencephalographic findings in neurosyphilis vary, depending on the type, area, and degree of involvement of the nervous system, the stage of the disease, the rate of progression of the disease process, and the age of the patient (Arentsen and Voldby, 1952; Kiloh et al., 1972). Patients with tabes dorsalis or spinal cord disease usually show little or no electroencephalographic abnormality (Arentsen and Voldby, 1952). Patients with syphilis that involves the CNS, meningovascular syphilis, general paresis, or optic atrophy may show disorganization and slowing of the background, a monorhythmic theta pattern, or bursts of delta waves (Arentsen and Voldby, 1952; Kiloh et al., 1972; Kooi et al., 1978; Radermecker, 1977).
The slow-wave abnormalities often occur in a diffuse fashion, with the maximal emphasis over the anterior head regions (Arentsen and Voldby, 1952). At times, more focal slow-wave abnormalities and epileptiform discharges are present, particularly in patients with meningovascular syphilis (Kooi et al., 1978). In general, there is a relationship between the degree of electroencephalographic abnormalities and the degree of mental involvement, and the electroencephalographic pattern often becomes more abnormal as the disease progresses (Radermecker, 1977). Age also is a factor, in that younger patients tend to show a greater degree of abnormality than do older patients (Arentsen and Voldby, 1952).
After treatment, there is a decrease in the electroencephalographic abnormalities that parallels the clinical improvement. On occasion, some residual abnormalities may be present in patients with late inactive disease, and, conversely, neurological and psychological sequelae can be present despite a return to a normal electroencephalographic pattern (Radermecker, 1977).
In infants with congenital syphilis, the EEG may show slowing, asymmetry, focal or multifocal epileptiform abnormalities, or hypsarrhythmia (Dreyfus-Brisac and Ellingson, 1972).
Behçet’s Disease
In neuro-Behçet’s disease (uveomeningitis), the EEG usually shows some abnormality when pleocytosis of the spinal fluid is present (Vinken and Bruyn, 1978a). Paroxysmal slow-wave abnormalities and delta slowing are seen with more severe involvement of the CNS (Vinken and Bruyn, 1978a). Although the EEG abnormalities may not be related to the symptomatology, there is a correlation with the course of the disease, and progressive EEG abnormalities are seen in patients who show a deterioration (Vinken and Bruyn, 1978a).
Multiple Sclerosis
The incidence of electroencephalographic abnormalities in multiple sclerosis as reported in the literature varies from 20% to 50%, depending on the location of the CNS involvement, the stage of the disease, and the criteria used (Kiloh et al., 1972; Kooi et al., 1978; Lević, 1978). The electroencephalographic abnormalities, when present, usually consist of varying degrees of nonspecific slowing that may occur in a focal or diffuse manner. The abnormalities are more likely to be seen during periods of exacerbation and often resolve during periods of remission (Kooi et al., 1978). Patients with mental dysfunction may show moderate degrees of slow-wave abnormalities (Kooi et al., 1978) (Fig. 16.10). At times, focal electroencephalographic abnormalities may be present and show some correlation with the area of maximal cerebral involvement; more often, however, there is little correlation between the electroencephalographic findings and the clinical findings (Kiloh et al., 1972; Kooi et al., 1978; Lević, 1978). In rare instances, epileptiform abnormalities have been seen; however, in general, seizures are uncommon in patients with multiple sclerosis (Kiloh et al., 1972; Kooi et al., 1978). Periodic lateralized discharges have also been noted in patients with multiple sclerosis (Awerbuch and Verma, 1987; Chabolla et al., 1996).
Figure 16.10. EEG showing generalized slowing in a 44-year-old woman with multiple sclerosis who has impaired mentation.

More useful than the EEG are the evoked potential studies in suggesting or confirming the presence of a demyelinating process affecting various areas of the nervous system (Kooi et al., 1978; Stockard and Sharbrough, 1980); this is discussed in more detail in the section on evoked potentials.
Prenatal Infections
Infections can affect the fetus at any stage of development. Infections that occur in the fetus during the first trimester cause congenital defects, developmental arrest, or organ malformations; those that occur near or at term produce effects similar to those seen with postnatal infections (Dreyfus-Brisac and Ellingson, 1972). The types of EEG abnormalities reflect the type and degree of CNS involvement rather than the specific type of infectious process. Sharp waves and high-voltage slow-wave activity are more likely to be seen with an encephalitic process. A low-voltage or almost flat tracing may be seen with hydranencephaly; a focal area of suppression can occur with porencephaly, and hypsarrhythmia can develop in any infant with a severe insult to the CNS (Dreyfus-Brisac and Ellingson, 1972). Although most infants with prenatal brain damage show some type of EEG abnormality, this may not be apparent at birth or may be present only during the sleep recording (Dreyfus-Brisac and Ellingson, 1972).
Neonatal Meningoencephalitis
In neonatal meningoencephalitis, the EEG is usually abnormal and shows the presence of focal or multifocal spikes or sharp waves, clinical and subclinical electrographic seizure discharges, theta or delta rhythms, or depression of activity (Dreyfus-Brisac and Ellingson, 1972). In infants who recover, the EEG shows a progressive improvement, although there may be a lag. In patients in whom the EEG remains abnormal, the infant either dies or is left with a residual deficit (Dreyfus-Brisac and Ellingson, 1972). Although the EEG findings are not specific for meningoencephalitis, as these types of findings can be seen with any severe insult to the neonatal CNS, serial recordings can be helpful in indicating the course of the disease, determining the severity of the cerebral damage, and predicting the development of sequelae (Dreyfus-Brisac and Ellingson, 1972).
Hemiconvulsions, Hemiplegia, and Epilepsy
In the hemiconvulsions, hemiplegia, and epilepsy (HHE) syndrome, the infant presents with a series of hemiconvulsions or with hemiconvulsive status during an acute febrile illness (Gastaut et al., 1959/1960). Following this, the patient is left with a flaccid hemiparesis that evolves into a spastic hemiplegia. Later the child has the onset of chronic epilepsy, most often arising from the temporal lobe (Gastaut et al., 1959/1960). The HHE syndrome may occur from birth up to 4 years of age but is most commonly seen between 6 months and 2 years of age. The EEG in the acute stages shows frequent or continuous spike or spike-and-wave discharges over the involved side and may have some reflection to the contralateral side (Gastaut et al., 1959/1960). After the acute stages of seizures, there is a reduction in the activity over the involved side. In later recordings, there is a persistent attenuation of activity over the affected hemisphere, as well as the occurrence of focal or multifocal epileptiform discharges (Fig. 16.11). At times, bilateral discharges may be present, but with a decreased amplitude over the affected side (Gastaut et al., 1959/1960).
Figure 16.11. EEG of a 3-year-old child with the HHE syndrome showing left frontal spikes and attenuation of the background activity over the left hemisphere.
Brain Abscess
Brain abscesses may occur as a result of meningitis, septicemia, or septic emboli, or as an extension of an infectious process involving the ears, mastoids, and sinuses. In the early stages of an acute supratentorial abscess, the EEG may show diffuse slowing with a poorly defined focus. This pattern is more likely to occur with meningoencephalitis, if the patient is obtunded, and when the more focal abnormalities are obscured by generalized slow-wave abnormalities. Focal slowing becomes more apparent as the suppurative process becomes localized (Fig. 16.12); marked focal polymorphic delta slowing can develop overlying the site of the abscess, particularly if the lesion is located close to the surface of the brain. Focal attenuation or suppression of activity can also be seen (Pine et al., 1952). If there are multiple abscesses, multiple electroencephalographic foci may be present (Scott, 1976). More generalized, intermittent, or shifting bursts of rhythmic slow waves (that is, a projected rhythm) also may be present; these bursts may be seen with a disturbance of the frontal lobe (Michel et al., 1979) or as a secondary effect of the mass lesion on midline structures. On infrequent occasions, focal or lateralized periodic sharp- or slow-wave complexes (periodic lateralized epileptiform discharges) may be present over the involved area of the brain, probably reflecting a rapid expansion of the lesion (LeBeau and Dondey, 1959).
Figure 16.12. EEG showing focal delta slowing over the right frontal region in a 9-year-old boy with a right frontal abscess.

In general, the degree of electroencephalographic abnormalities reflects the severity of the inflammatory process. The electroencephalographic changes seen with an acute focal supratentorial abscess are often more pronounced than those seen with other focal cerebral lesions; this difference can be helpful in suggesting or confirming the presence of an abscess (Scott, 1976). It has been stated that between 90% and 95% of all patients with a supratentorial abscess will have some type of electroencephalographic abnormality (Scott, 1976), and that the EEG is helpful in localizing the site of the abscess in 70% (Kiloh et al., 1972).
Infratentorial abscesses produce less severe slow-wave abnormalities, and at times there may be little or no change on the EEG. When present, the slow-wave abnormalities usually consist of bilaterally synchronous or shifting groups of intermittent rhythmic slow waves (Kooi et al., 1978).
Chronic abscesses develop more slowly and insidiously and often without overt clinical signs of the infectious process. These are usually well-encapsulated abscesses that develop after the initial infection has been cured (Radermecker, 1977). A chronic abscess behaves like a progressive mass lesion and shows the same type of electroencephalographic findings as a tumor (that is, focal slow-wave abnormalities, asymmetry, or attenuation of the background activity), and, if there is increased intraventricular pressure, diffuse intermittent rhythmic slow-wave abnormalities. If the abscess develops very slowly, only minor or subtle electroencephalographic changes may be present.
After treatment, the slow-wave abnormalities improve; however, the EEG rarely returns to normal (Kooi et al., 1978). If surgical intervention is used, the postoperative EEGs show a rapid decrease in the degree of slow-wave abnormalities within the first few days after surgery; however, some slowing and asymmetry of activity often continues to be present over the surgical area. Epileptiform abnormalities are not very common in the acute stages of the abscess; however, about 75% of patients with cerebral abscesses subsequently suffer seizures (Legg et al., 1973; Scott, 1976), and those patients in whom the amount of epileptiform activity increases within the first 1 to 5 years have a greater tendency of developing subsequent seizures (Legg et al., 1973; Scott, 1976).
Subdural Empyema
An empyema is a localized focus of infection in the subdural space that usually develops from a local propagated infection and can spread easily, making it an even more serious infectious process than an abscess. The EEG in the early stages may show a poorly defined focus. Later, more distinct focal slow-wave abnormalities develop, together with focal epileptiform discharges, indicating an irritative cortical focus. As with a subdural hematoma, there is often an attenuation or suppression of background activity over the side of the empyema.
Thrombophlebitis of the dural veins can occur as a result of sepsis, a contiguous infection, or septic embolization. When this affects the superior lateral sinus, the patient often presents with a headache, seizures, paresis, and increased intracranial pressure (Radermecker, 1977). The EEG during the acute phases may show diffuse slowing with focal emphasis, bifrontal delta slowing, a reduction of the amplitude of the activity over the involved side, epileptiform abnormalities, or, at times, subclinical electrographic status (Lemmi and Little, 1960; Radermecker, 1977). Later EEGs show a residual asymmetry, persistent slow-wave abnormalities, and epileptiform activity (Lemmi and Little, 1960).
In thrombophlebitis of the lateral sinus, the EEG shows lateralized slowing and focal epileptiform abnormalities (Lemmi and Little, 1960; Radermecker, 1977).
Thrombosis of the superficial cortical veins often results in focal seizures and a focal neurological deficit, with the EEG showing focal slowing and epileptiform abnormalities over the involved area (Lemmi and Little, 1960; Radermecker, 1977).
Summary and Conclusions
Although the EEG shows a variety of patterns in association with various inflammatory processes, the EEG can help to (a) confirm and indicate the degree and extent of CNS involvement by the inflammatory process; (b) make the diagnosis of herpes simplex encephalitis, Creutzfeldt-Jakob disease, and SSPE when the characteristic electroencephalographic pattern of these diseases is present; (c) indicate the presence of a focal lesion; (d) monitor the course of the disease process; and (e) detect the development of complications or sequelae.
Aguilar, M.J., and Rasmussen, T. 1960. Role of encephalitis on the pathogenesis of epilepsy. Arch. Neurol. 2:663–676.
Andermann, F. 1991. Chronic Encephalitis and Epilepsy. Rasmussen’s Syndrom e. Toronto: Butterworth-Heinemann.
Andrews, P.I., Dichter, M.A., Berkovic, S.F., et al. 1996. Plasmapheresis in Rasmussen’s encephalitis. Neurology 46:242–246.
Andrews, P.I., McNamara, J.O., and Lewis, D.V. 1997. Clinical and electroencephalographic correlates in Rasmussen’s encephalitis. Epilepsia 38:189–194.

Aoki, Y., and Lombroso, C.T. 1973. Prognostic value of electroencephalography in Reye’s syndrome. Neurology (Minneapolis) 23:333–343.
Arentsen, K., and Voldby, H. 1952. Electroencephalographic changes in neurosyphilis. Electroencephalogr. Clin. Neurophysiol. 4:331–337.
Au, W.J., Gabor, A.J., Vijayan, N., et al. 1980. Periodic lateralized epileptiform complexes (PLEDs) in Creutzfeldt-Jakob disease. Neurology 30: 611–618.
Awerbuch, G.I., and Verma, N.P. 1987. Periodic epileptiform discharges in a patient with definite multiple sclerosis. Clin. Electroencephalogr. 18: 38–40.
Bernad, P.G. 1991. The neurological and electroencephalographic changes in AIDS. Clin. Electroencephalogr. 22:65–70.
Brown, P., Rodgers-Johnson, P., Cathala, F., et al. 1984. Creutzfeldt-Jakob disease of long duration: Clinocopathological characteristics, transmissibility, and differential diagnosis. Ann. Neurol. 16:295–304.
Burger, L.J., Rowan, A.J., and Goldensohn, E.S. 1972. Creutzfeldt-Jakob disease. An electroencephalographic study. Arch. Neurol. 26:428–433.
Chabolla, D.R., Moore, J.L., and Westmoreland, B.F. 1996. Periodic lateralized epileptiform discharges in multiple sclerosis. Electroencephalogr. Clin. Neurophysiol. 98:5–8.
Chaves-Carballo, E., Gomez, M.R., and Sharbrough, F.W. 1975. Encephalopathy and fatty infiltration of the viscera (Reye-Johnson syndrome). A 17-year experience. Mayo Clin. Proc. 50:209–215.
Ch’ien, L.T., Boehm, R.M., Robinson, H., et al. 1977. Characteristic early electroencephalographic changes in herpes simplex encephalitis. Clinical and virologic studies. Arch. Neurol. 34:361–364.
Cobb, W. 1966. The periodic events of subacute sclerosing leucoencephalitis. Electroencephalogr. Clin. Neurophysiol. 21:278–294.
Cobb, W.A. 1975. Electroencephalographic changes in viral encephalitis. In Viral Diseases of the Central Nervous System, Ed. L.S. Illis, pp. 76–89, Baltimore: Williams & Wilkins.
Cobb, W., and Hill, D. 1950. Electroencephalogram in subacute progressive encephalitis. Brain 73:392–404.
Cobb, W.A., Hornabrook, R.W., and Sanders, S. 1973. The EEG of kuru. Electroencephalogr. Clin. Neurophysiol. 34:419–427.
Desmond, M.M., Wilson, G.S., Melnick, J.L., et al. 1967. Congenital rubella encephalitis: course and early sequelae. J. Pediatr. 71:311–331.
Dreyfus-Brisac, C., and Ellingson, R.J. 1972. Hereditary, congenital and perinatal diseases. In Handbook of Electroencephalography and Clinical Neurophysiology, vol. 15, part B, Ed.-in-chief, A. Remond. Amsterdam: Elsevier.
Drury, I., and Beydou, A. 1996. Evolution of periodic complexes in Creutzfeldt-Jakob disease. Am. J. End. Technol. 36:230–234.
Elian, M. 1975. Herpes simplex encephalitis. Prognosis and longterm follow-up. Arch. Neurol. 32:39–43.
Elliott, F., Gardner-Thorpe, C., Barwick, D.D., et al. 1974. Creutzfeldt-Jakob disease. Modification of clinical and electroencephalographic activity with methylphenidate and diazepam. J. Neurol. Neurosurg. Psychiatry 37:879–887.
Enzensberger, W., Helm, E.B., and Fischer, P.-A. 1986. EEG follow-up examinations in AIDS patients. Electroencephalogr. Clin. Neurophysiol. 63:28P(abst).
Furlan, A.J., Henry, C.E., Sweeney, P.J., et al. 1981. Focal EEG abnormalities in Heidenhain’s variant of Creutzfeldt-Jakob disease. Arch. Neurol. 38:312–314.
Gaches, J., and Arfel, G. 1972. Certitude et suspicions d’encéphalites herpétiques. Aspects électroencéphalographiques. Encephale 61:510–549.
Gajdusek, D.C., and Zigas, V. 1957. Degenerative disease of the central nervous system in New Guinea. N. Engl. J. Med. 257:974–978.
Gastaut, H., and Miletto, G. 1955. Interprétation physiopathogénique de la rage furieuse. Rev. Neurol. (Paris) 92:1–25.
Gastaut, H., Poirier, F., Payan, H., et al. 1959/1960. H.H.E. Syndrome, hemiconvulsions, hemiplegia, epilepsy. Epilepsia 1:418–447.
Gibbs, F.A., Gibbs, E.L., Carpenter, P.R., et al. 1959. Electroencephalographic abnormality in “uncomplicated” childhood diseases. JAMA 171:1050–1055.
Gibbs, F.A., Gibbs, E.L., Spies, H.W., et al. 1964. Common types of childhood encephalitis. Electroencephalographic and clinical relationships. Arch. Neurol. 10:1–11.
Gloor, P. 1980. EEG characteristics in Creutzfeldt-Jakob disease. Arch. Neurol. 8:341.
Gloor, P., Kalabay, O., and Giard, N. 1968. The electroencephalogram in diffuse encephalopathies. Electroencephalographic correlates of grey and white matter lesions. Brain 91:779–802.
Grabow, J.D., Matthews, C.G., Chun, R.W.M., et al. 1969. The electroencephalogram and clinical sequelae of California arbovirus encephalitis. Neurology (Minneapolis) 19:394–404.
Greenberg, D.A., Weinkle, D.J., and Aminoff, M.J. 1982. Periodic EEG complexes in infectious mononucleosis encephalitis. J. Neurol. Neurosurg. Psychiatry 45:648–651.
Gupta, P.C., and Seth, P. 1973. Periodic complexes in herpes simplex encephalitis. A clinical and experimental study. Electroencephalogr. Clin. Neurophysiol. 35:67–74.
Hanzel, F. 1961. Aspects of tick encephalitis. In Encephalitides, Eds. L. Van Bogaert, J. Radermecker, J. Hazay, et al., pp. 661–670. Amsterdam: Elsevier.
Illis, L.S., and Taylor, F.M. 1972. The electroencephalogram in herpes-simplex encephalitis. Lancet 1:718–721.
Jay, V., Becker, L.E., Ostubo, H., et al. 1995. Chronic encephalitis and epilepsy (Rasmussen’s encephalitis): detection of cytomegalovirus and herpes simplex virus 1 by the polymerase chain reaction and in situ hybridization. Neurology 45:108–117.
Johnson, D.A., Klass, D.W., and Millichap, J.G. 1964. Electroencephalogram in Sydenham’s chorea. Arch. Neurol. 10:21–27.
Jones, D.P., and Nevin, S. 1954. Rapidly progressive cerebral degeneration (subacute vascular encephalopathy) with mental disorder, focal disturbances, and myoclonic epilepsy. J. Neurol. Neurosurg. Psychiatry 17: 148–159.
Kiloh, L.G., McComas, A.J., and Osselton, J.W. 1972. Clinical Electroencephalography, 3rd ed. London: Butterworths.
Klatzman, D., et al. 1984. Selective tropism of lymphadenopathy associated virus (LAV) for helper-inducer lymphocytes. Science 225:59–63.
Klein, C., Kimiagar, I., Pollak, L., et al. 2002. Neurological features of West Nile Virus infection during the 2000 outbreak in a regional hospital in Israel. J. Neurol. Sci. 200:63–66.
Kooi, K.A., Tucker, R.P., and Marshall, R.E. 1978. Fundamentals of Electroencephalography, 2nd ed. Hagerstown, MD: Harper & Row.
Lavy, S., Lavy, R., and Brand, A. 1964. Neurological and electroencephalographic abnormalities in rheumatic fever. Acta Neurol. Scand. 40:76–88.
LeBeau, J., and Dondey, M. 1959. Importance diagnostique de certaines activités électrecéphalographiques latéralisées, périodiques ou à tendance périodique au cours des abcès du cerveau. Electroencephalogr. Clin. Neurophysiol. 11:43–58.
Legg, N.J., Gupta, P.C., and Scott, D.F. 1973. Epilepsy following cerebral abscess. A clinical and EEG study of 70 patients. Brain 96:259–268.
Lehtinen, I., and Halonen, J.-P. 1984. EEG findings in tick borne encephalitis. J. Neurol. Neurosurg. Psychiatry 47:500–504.
Lemmi, H., and Little, S.C. 1960. Occlusion of intracranial venous structures. Arch. Neurol. 3:252–266.
Lević, Z.M. 1978. Electroencephalographic studies in multiple sclerosis. Specific changes in benign multiple sclerosis. Electroencephalogr. Clin. Neurophysiol. 44:471–478.
Levy, R.M., and Bredesen, D.E. 1988. Central nervous system dysfunction in acquired immunodeficiency syndrome. In AIDS and the Nervous System, Eds. M.L. Rosenblum et al., pp. 29–63. New York: Raven Press.
Levy, S.R., Chiappa, K.H., Burke, C.J., et al. 1986. Early evolution and incidence of electroencephalographic abnormalities in Creutzfeldt-Jakob disease. J. Clin. Neurophysiol. 3:1–21.
Lombroso, C.T. 1968. Remarks on the EEG and movement disorder in SSPE. Neurology (Minneapolis) 18:69–75.
Markand, O.N., and Panszi, J.G. 1975. The electroencephalogram in subacute sclerosing panencephalitis. Arch. Neurol. 32:719–726.
May, W.W. 1968. Creutzfeldt-Jakob disease. I. Survey of the literature and clinical diagnosis. Acta Neurol. Scand. 44:1–32.
Metz, H., Gregoriou, M., and Sandifer, P. 1964. Subacute sclerosing panencephalitis. A review of 17 cases with special reference to clinical diagnostic criteria. Arch. Dis. Child. 39:554–557.
Michel, B., Gastaut, J.L., and Bianchi, L. 1979. Electroencephalographic cranial computerized tomographic correlations in brain abscess. Electroencephalogr. Clin. Neurophysiol. 46:256–273.
Mizrahi, E.M., and Tharp, B.R. 1982. A characteristic EEG pattern in neonatal herpes simplex encephalitis. Neurology 32:1215–1220.
Nelson, J.R., and Leffman, H. 1963. The human diffusely projecting system. Evoked potentials and interactions. Arch. Neurol. 8:544–556.
Nevin, S., McMenemey, W.H., Behrman, S., et al. 1960. Subacute spongiform encephalopathy. A subacute form of encephalopathy attributable to vascular dysfunction (spongiform cerebral atrophy). Brain 83:519–564.

Nicholson, J., Gross, G., Callaway, C., et al. 1986. In vitro infection of human monocytes with human T-lymphotropic virus type III/lymphadenopathy associated virus (HTLV-III/LAV). J. Immunol. 137:323–329.
Pachner, A.R., and Steere, A.C. 1985. The triad of neurologic manifestations of Lyme disease: meningitis, cranial neuritis, and radiculoneuritis. Neurology 35:47–53.
Pampiglione, G. 1964a. Polymyographic studies of some involuntary movements in subacute sclerosing pan-encephalitis. Arch. Dis. Child. 39: 558–563.
Pampiglione, G. 1964b. Prodromal phase of measles. Some neurophysiological studies. Br. Med. J. 2:1296–1300.
Pampiglione, G., Griffith, A.H., and Bramwell, E.C. 1971. Transient cerebral changes after vaccination against measles. Lancet 2:5–8.
Perot, P., Lloyd-Smith, D., Libman, I., et al. 1963. Trichinosis encephalitis: a study of electroencephalographic and neuropsychiatric abnormalities. Neurology 13:477–485.
Petre-Quadens, O., Sfaello, Z., van Bogaert, L., et al. 1968. Sleep study in SSPE (first results). Neurology (Minneapolis) 18:60–68.
Pettay, O., Leinikki, P., Donner, M., et al. 1972. Herpes simplex virus infection in the newborn. Arch. Dis. Child. 47:97–103.
Pine, I., Atoynatan, T.H., and Margolis, G. 1952. The EEG findings in 18 patients with brain abscess: case reports and a review of the literature. Electroencephalogr. Clin. Neurophysiol. 4:165–179.
Power, C., Poland, S.D., Blume, W.T., et al. 1990. Cytomegalovirus and Rasmussen’s encephalitis. Lancet 336:1282–1284.
Radermecker, F.J. (Ed.) 1977. Infections and Inflammatory Reactions, Allergy and Allergic Reactions; Degenerative Diseases/Handbook of Electroencephalography and Clinical Neurophysiology, vol. 15, part A. Ed.-in-chief, A. Remond. Amsterdam: Elsevier.
Radermecker, J. 1949. Aspects électroencéphalographiques dans trois cas d’encéphalite subaiguë. Acta Neurol. Psychiatr. Belg. 49:222–232.
Radermecker, J., and Poser, C.M. 1960. The significance of repetitive paroxysmal electroencephalographic patterns. Their specificity in subacute sclerosing leukoencephalitis. World Neurol. 1:422–431.
Rasmussen, T., and McCann, W. 1968. Clinical studies of patients with focal epilepsy due to “chronic encephalitis.” Trans. Am. Neurol. Assoc. 93:89–94.
Rawls, W.E., Dyck, P.J., Klass, D.W., et al. 1966. Encephalitis associated with herpes simplex virus. Ann. Intern. Med. 64:104–115.
Reiher, J., Lapointe, L.R., and Lessard, L. 1973. Prolonged and variable intervals between EEG complexes in subacute inclusion body encephalitis. Can. Med. Assoc. J. 108:729–732.
Rogers, S.W., Andrews, P.I., Gahring, L.C., et al. 1994. Autoantibodies to glutamate receptor GluR3 in Rasmussen’s encephalitis. Science 265: 648–651.
Sainio, K., Granstrom, M.L., Pettay, O., et al. 1983. EEG in neonatal herpes simplex encephalitis. Electroencephalogr. Clin. Neurophysiol. 56:556–561.
Schnell, R.G., Dyck, P.J., Bowie, E.J.W., et al. 1966. Infectious mononucleosis. Neurologic and EEG findings. Medicine 45:51–63.
Scott, D.F. 1960. Understanding EEG. An Introduction to Electroencephalography. London: Gerald Duckworth.
Smith, J.B., Westmoreland, B.F., Reagan, T.J., et al. 1975. A distinctive clinical EEG profile in herpes simplex encephalitis. Mayo Clin. Proc. 50:469–474.
Smith, J.B., Groover, R.V., Klass, D.W., et al. 1977. Multicystic cerebral degeneration in neonatal herpes simplex virus encephalitis. Am. J. Dis. Child. 131:568–572.
Snider, W.D., Simpson, D.M., Nielsen, S., et al. 1983. Neurological complications of acquired immune deficiency syndrome: analysis of 50 patients. Ann. Neurol. 14:403–418.
Stockard, J.J., and Sharbrough, F.W. 1980. Unique contributions of short-latency auditory and somatosensory evoked potentials to neurologic diagnosis. Prog. Clin. Neurophysiol. 7:231–263.
Tapie, P., Buguet, A., Tabaraud, F., et al. 1996. Electroencephalographic and polygraphic features of 24-hour recordings in sleeping sickness and healthy African subjects. J. Clin. Neurophysiol. 13:339–344.
Tietjen, G.E., and Drury, I. 1990. Familial Creutzfeldt-Jakob disease without periodic EEG activity. Ann. Neurol. 28:585–588.
Tinuper, P., de Carolis, P., Galeotti, M., et al. 1990. Electroencephalogram and HIV infection: a prospective study in 100 patients. Clin. Electroencephalogr. 21:3:145–150.
Turrell, R.C., and Roseman, E. 1955. Electroencephalographic studies of the encephalopathies. IV. Serial studies in meningococcic meningitis. Arch. Neurol. Psychiatr. 73:141–148.
Upton, A., and Gumpert, J. 1970. Electroencephalography in diagnosis of herpes-simplex encephalitis. Lancet 1:650–652.
Usher, S.J., and Jasper, H.H. 1941. The etiology of Sydenham’s chorea. Electroencephalographic studies. Can. Med. Assoc. J. 44:365–371.
Vinken, P.J., and Bruyn, G.W. (Eds.) 1978a. Infections of the Nervous System, Part 2. Neurology, vol. 34. Amsterdam: North-Holland.
Vinken, P.J., and Bruyn, G.W. (Eds.) 1978b. Infections of the Nervous System. Part 3. Neurology, vol. 35. Amsterdam: North-Holland.
Westmoreland, B.F., Gomez, M.R., and Blume, W.T. 1977. Activation of periodic complexes of subacute sclerosing panencephalitis by sleep. Ann. Neurol. 1:185–187.
Westmoreland, B.F., Sharbrough, F.W., and Donat, J.R. 1979. Stimulus-induced EEG complexes and motor spasms in subacute sclerosing panencephalitis. Neurology (Minneapolis) 29:1154–1157.
Will, R.G., Ironside, J.W., Zeidler, M., et al. 1996. A new variant of Creutzfeldt-Jakob disease in the UK. Lancet 347:921–925.
Wolinsky, J.S., Berg, B.O., and Maitland, C.J. 1976. Progressive rubella panencephalitis. Arch. Neurol. 33:722–723.
Wulff, C.H. 1982. Subacute sclerosing panencephalitis: serial electroencephalographic recordings. J. Neurol. Neurosurg. Psychiatry 45:418–421.
Zerr, I., Schultz-Schaeffer, W.J., Giese, A., et al. 2000. Current clinical diagnosis in Creutzfeldt-Jakob disease: identification of uncommon variants. Ann. Neurol. 48:323–329.
Zschocke, S. 1987. EEG und Intensivüberwachung. Presented at EEG Course, German EEG Society, Munich, March 1987.