Textbook Continuous Eeg Monitoring Principles and Practice 1St Edition Aatif M Husain Ebook All Chapter PDF
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Continuous
EEG Monitoring
Aatif M. Husain
Saurabh R. Sinha
Editors
123
Continuous EEG Monitoring
Aatif M. Husain • Saurabh R. Sinha
Editors
Continuous EEG
Monitoring
Principles and Practice
Editors
Aatif M. Husain Saurabh R. Sinha
Neurology Neurology
Duke University Medical Center Duke University Medical Center
Durham Durham
North Carolina North Carolina
USA USA
v
Preface
It was only 20 years ago that when continuous EEG (cEEG) monitoring was dis-
cussed, it was in the context of monitoring patients in the epilepsy monitoring unit
for spell characterization or epilepsy surgery evaluation. Certainly EEGs were per-
formed in the intensive care units (ICU), and patients even underwent “prolonged
monitoring.” However, in the era of paper EEGs, prolonged monitoring often con-
sisted of turning the EEG machine on for 5 min every hour or so. Interpretation of
reams of paper was done the following day. Partly because of what now appears to
be rudimentary methods, we did not appreciate the extraordinary prevalence of sei-
zures in critically ill patients.
The last two decades have seen a remarkable change in our understanding of sei-
zures in critically ill patients. Much of this change has been due to the availability of
cEEG monitoring. The advent of digital EEG and advances in information technol-
ogy have paved the way for the broad availability of cEEG monitoring, which has led
to the realization that about 20 % of critically ill patients in whom cEEG monitoring
is performed have seizures or status epilepticus (SE). The medical community has
recognized the need for cEEG monitoring in large and small, university and com-
munity hospitals, and this has fueled a remarkable demand for these services.
Continuous EEG monitoring has now become a discipline in its own right. A few
years ago, a handful of like-minded individuals set up the Critical Care EEG
Monitoring and Research Consortium (CCEMRC); this consortium has grown to
about 50 members. Many clinical neurophysiology fellowships have made cEEG
monitoring education an essential part of their training. In fact, dedicated cEEG
monitoring fellowships have also become available. Many clinical neurophysiolo-
gists and neurointensivists now complete their training with a special interest and
expertise in cEEG monitoring. Professional societies throughout the world have
also started offering education and training in this discipline at their annual meet-
ings. The American Board of Clinical Neurophysiology now offers a subspecialty
certification in critical care EEG monitoring.
This remarkable growth in cEEG monitoring was the impetus behind this book.
The ever-expanding knowledge base, advances in recording and analysis, interpre-
tation and treatment concerns, and implementation challenges can best be addressed
in a textbook on this subject. In an effort to address these challenges and provide a
state of the art of this field, we undertook editing Continuous EEG Monitoring:
Principles and Practice.
vii
viii Preface
patients. It is through their illness that we learn. It is this learning that we hope will
provide more effective treatment for these and other patients.
Finally, we must thank our families. Medicine is an extremely fulfilling and
demanding profession. Our spouses and children endure our long work hours rou-
tinely; this book added many more hours away from them. Without their constant
support, encouragement, and motivation, none of this would have been possible. For
that, and a lot more, we are forever grateful.
xi
xii Contents
Index������������������������������������������������������������������������������������������������������������������ 657
About the Editors
Saurabh R. Sinha, MD, PhD is associate professor and vice-chair for education,
Department of Neurology, Duke University Medical Center, and director of the
Epilepsy Monitoring Unit, Duke University Hospital. After receiving his B.Sc. in
biomedical engineering from Johns Hopkins University in Baltimore, Maryland, he
completed his M.D., Ph.D. (in neuroscience), and internship (internal medicine) at
Baylor College of Medicine in Houston, Texas. Dr. Sinha completed his residency
in neurology and fellowships in clinical neurophysiology and advanced epilepsy at
Johns Hopkins Hospital. After 4 years as medical director of the Epilepsy Program
at Sinai Hospital in Baltimore, Dr. Sinha joined Duke University Medical Center
where he currently also serves as program director for the Neurology Residency.
His clinical and research interests include surgical epilepsy, quantitative EEG anal-
ysis, and neurophysiologic intraoperative monitoring. Dr. Sinha is currently on the
board of directors for the American Board of Registration of EEG and EP
Technologists and the American Board of Clinical Neurophysiology and on the
council of the American Clinical Neurophysiology Society.
xv
Part I
Clinical Aspects
The History of Continuous EEG
Monitoring 1
Raoul Sutter and Peter W. Kaplan
Contents
Introduction.................................................................................................................................. 4
From the Galvanometer to Scalp Electrodes................................................................................ 4
The First Human EEG................................................................................................................. 6
Early Use of Multichannel EEG.................................................................................................. 6
From Paper to Digital Recording................................................................................................. 7
Diagnosis and Prognosis.............................................................................................................. 8
Directing Treatment..................................................................................................................... 9
Interinstitutional Variability....................................................................................................... 10
Future Perspectives.................................................................................................................... 11
Conclusions................................................................................................................................ 11
References.................................................................................................................................. 11
R. Sutter, MD (*)
Clinic of Intensive Care Medicine and Division of Clinical Neurophysiology,
Department of Neurology, University Hospital Basel,
Petersgraben 4, Basel CH – 4031, Switzerland
e-mail: [email protected]
P.W. Kaplan, MB BS, FRCP
Department of Neurology, Johns Hopkins Bayview Medical Care Center,
301 Building, 4940 Eastern Avenue, Baltimore, MD 21224, USA
e-mail: [email protected]
Introduction
The history of electroencephalography (EEG) began in the late 1800s and has
increasingly led to clinical, experimental, and computational studies that have
enabled the discovery, understanding, recognition, diagnosis, and treatment of a
great number of neurophysiological abnormalities and critical illnesses of the brain
and spinal cord. Currently, EEGs are often continuously recorded mostly using
scalp or cortical electrodes with enough digital EEG memory to store extended
recordings of several hours. Modern EEG machines are further equipped with fully
computerized signal processing systems allowing rapid and multidimensional anal-
yses that present many challenges to the managing physicians.
In this chapter, we provide an overview of the history of EEG and its clinical
contributions toward the field of continuous EEG monitoring in critical care.
Milestones in the history of EEG and the emergence of continuous EEG monitoring
are presented in Fig. 1.
The introduction of the galvanometer with astatic needles has been mainly associ-
ated with Leopoldo Nobili, a physicist in Florence, and was further refined in 1858
by William Thompson (Lord Kelvin) in England. Galvanometers were able to faith-
fully demonstrate continuous electrical currents and their variations in intensity, but
could not detect extremely brief electrical phenomena (Fig. 2). In 1875, Richard
Caton, a scientist from Liverpool, England, placed two electrodes of a galvanometer
over the scalp of a human and became the first to record brain activity in the form of
electrical signals. Caton used a beam of light projected on the mirror of the galva-
nometer and reflected onto a large scale placed on the wall. With this type of visu-
alization, Caton found that “feeble currents of varying direction pass through the
multiplier when the electrodes are placed at two points of the external scalp
Electric Multichannel
stimulation of recordings
cerebral cortex
1870 1900 1910 1920 1930 1940 1950 1960 1970 1980 1990 2000
time
Scale
Spring
Pointer
Conductor terminal
Inductor
Magnet
Conductor terminal
surface.” This initial experiment led to the concept of the graphic recording of reg-
istered electrical brain signals, the technique that underlies present-day EEG. Caton
noted that the surface of the gray matter was positively charged with respect to
deeper structures in the cerebrum. He also noted that the electric currents of the
cerebrum changed in relation to the underlying function with neurofunctional active
regions exhibiting negative variations of electric current. Hence, Caton has also
been credited with pioneering the work on evoked potentials.
Concurrent with Caton’s work, physiologists in Eastern Europe began to report
their observations on cerebral electrical activity with another discovery of greater
impact on the neuroscientific world – the capability of the cerebral cortex to be
electrically stimulated as described by Gustav Fritsch and Julius Eduard Hitzig in
1870. These discoveries were followed by several observations of spontaneous elec-
trical activity in the brains of animals and the studies of electrical responses of the
human brain after electrical stimulation. These included the first EEG evidence of
epileptic activity during a seizure in a dog following electrical stimulation reported
by Napoleon Cybulski, a Polish physiologist. Seven years after the study of Fritsch
and Hitzig, Vasili Y. Danilevsky wrote his thesis on electrical stimulation and the
spontaneous electrical activity of animal brains while working at the University of
Kharkov. However, Danilevsky was disappointed as he had expected better correla-
tion of the spontaneous regional electrical brain activity with psychic and emotional
processes. Adolf Beck, a Polish physician and physiologist at the University of
Lwów, Poland, further investigated the spontaneous electrical brain activity of
6 R. Sutter and P.W. Kaplan
rabbits and dogs using nonpolarizable electrodes and observed the disappearance of
rhythmical oscillations during illumination of the eyes (i.e., “alpha blocking”).
In 1903, Willem Einthoven, a Dutch doctor and physiologist, invented a string
galvanometer, an instrument with greater sensitivity of detection but which required
photographic recording. The string galvanometer became the standard instrument
for EEG at the turn of the century with Pravdich-Neminsky, a Ukrainian and then
Soviet physiologist, reporting electrical activity recordings using this technique in
animal brains in 1912.
In the 1920s, Hans Berger, a German neuropsychiatrist and the discoverer of the
human EEG, was the first to describe the existence of human EEG signals [1].
Berger first used a string galvanometer in 1910, to later migrate to an Edelmann
model followed by a more powerful Siemens double-coil galvanometer.
Unfortunately, it took more than 10 years for the scientific community to accept
these scalp potentials as genuine brain signals.
In 1926, Berger started to use the more powerful Siemens double-coil galvanom-
eter and published his first report of a human 3-min EEG recording in 1929. He
described the alpha rhythm as the dominant component of human EEG signals and
the alpha blocking response, a milestone in the history of clinical EEG [1]. For his
one-channel EEG tracings, Berger used a bipolar recording technique with fronto-
occipital leads along with a time marking line generated with a sine wave of 10
cycles/sec (Fig. 3). During the 1930s, Berger recorded the first EEG of human sleep,
detecting sleep spindles. He followed this with the examination of human EEG pat-
terns in hypoxic brain injury, in epilepsy, in the investigation of several diffuse and
localized brain dysfunctions, and with the examination of changes in EEG signals
with mental activities.
Since the first human EEG recordings in the early 1920s and their widespread accep-
tance 20 years later, it has been known that the amplitude and frequency content of
EEG patterns reveals substantial information about the neurofunctional state of the
brain. For example, the voltage record during deep sleep has dominant frequencies in
the delta range near 1 Hz, whereas the eyes-closed waking state is associated with
8 R. Sutter and P.W. Kaplan
sinusoidal oscillations of an alpha frequency range near 10 Hz. Early in the history
of EEG, it became clear that more standardized and automatic quantitative analyses
would allow for reliable identification and correlation of EEG information to differ-
ent neurofunctional states, such as distinguishing different sleep stages, determining
the depth of anesthesia, identifying waxing and waning epileptic activity during sei-
zures, and the analysis of encephalopathic states. Hence, in the 1950s, EEG became
widely available, and almost every tertiary academic medical care center had at least
one EEG machine. At the end of the decade, EEG was also in use in a large number
of nonacademic hospitals and private practices in the 1960s.
This propagation of EEG significantly slowed in the 1970s, possibly explained
by the advances in high resolution, structural neuroimaging techniques including
computed tomography and magnetic resonance imaging. However, it soon became
recognized that EEG provides real-time information on the neurofunctional status
and its spatial development that cannot be assessed at bedside by neuroimaging
techniques, and EEG regained interest in the 1990s.
Although in the 1980s technical advances allowed the EEG to be digitized and
recorded on videotape, the number of channels and the resolution were limited at
first. Electronic data storage volumes increased significantly in the 1990s, and
computer networking enabled remote EEG reading and simultaneous video record-
ing of the patients, making continuous EEG (cEEG) recordings over hours to days
of many critically ill patients, possible. As manual review and interpretation of
cEEG became increasingly labor-intensive, effective methods were developed to
assist in rapid and accurate EEG interpretation, especially regarding seizure detec-
tion. In the late 1990s and early 2000s, complex algorithms enabling quantitative
EEG analyses, such as the Wavelet analysis and Fourier analysis, with new focus
on shared activity between rhythms including phase synchrony and magnitude syn-
chrony, were developed. Automated spectral analysis was introduced to study
spectral content through a spectrogram also known as a time-frequency plot, a
color plot providing the temporal evolution of the EEG frequency spectrum. In this
context, the color provides information about the power at a given instant of time
for a given frequency band. These modern methods of EEG concerned with both
temporal and spatial properties revealed robust electrographic correlations with
cognitive processes, such as mental calculation, working memory, and selective
attention further expanding the yield of EEG and increasing the diagnostic power
of cEEG monitoring especially in epilepsy clinics and intensive care units (ICU) in
the last several years.
Critically ill patients often become confused or obtunded from a variety of critical
illnesses, including acute brain lesions, systemic metabolic derangements, seizures,
or status epilepticus (SE). Nonconvulsive seizures (NCS) and nonconvulsive status
epilepticus (NCSE) are states without visible convulsions and hence depend on
EEG and cEEG to both make a diagnosis and ascertain treatment success. In recent
The History of Continuous EEG Monitoring 9
Directing Treatment
Interinstitutional Variability
The widespread and increasing use of cEEG in recent years calls for a standardized
procedure to assure and enhance the quality of cEEG-related science. Data describ-
ing the current interinstitutional variability of cEEG practice in the critically ill are
limited. In a recent study, a survey of cEEG indications and procedures was sent to
intensivists and neurophysiologists responsible for ICU-cEEG at 151 institutions in
the USA [16]. At some institutions only one physician could be identified. Of the
137 physicians from 97 institutions who completed the survey, cEEG was used by
nearly all respondents to detect NCS or NCSE in patients with altered mental status
following clinical seizures with in intracerebral hemorrhage, after traumatic brain
injury and after cardiac arrest. It has also been used to characterize abnormal move-
ments suspected of being seizures.
The majority of physicians monitor comatose patients for 24–48 h. However,
in an ideal situation with unlimited resources, 18 % of respondents would increase
cEEG duration. Eighty-six percent of institutions have an on-call EEG technolo-
gist available 24/7 for new patient hookups, but only 26 % have technologists
available 24/7 in-house. There is substantial variability in who reviews EEGs and
how frequently the record is reviewed as well as how often quantitative EEG is
used. Although there is general agreement regarding the indications for cEEG in
ICUs, there is substantial interinstitutional variability on how the procedure is
performed. Future studies and guidelines in this context are warranted to justify
the increased use of cEEG in the ICUs and to improve the art and science of this
emerging field.
The History of Continuous EEG Monitoring 11
Future Perspectives
Nowadays, EEGs in ICUs are recorded invasively and noninvasively using entirely
computerized systems. The EEG machines are equipped with a variety of signal
processing software and enough memory for long-term recordings lasting several
hours or days. Delicate needle electrodes can be used for EEG recordings from the
cortex without the attenuation and nonlinearity effects of the skull. In the future,
EEG machines may be increasingly integrated with other dynamic neuroimaging
systems such as functional magnetic resonance imaging. However, to what extent
this development will target critical care is unclear and will face many obstacles
including the transportation of vulnerable, critically ill patients to the radiologic
units. New software for more complex investigations of neuronal network interac-
tion and for automated seizure detection and artifact suppression will emerge,
enhancing the scope and quality of application but also providing increasing ana-
lytic and technological challenges to neurophysiologists.
Conclusions
Within the span of approximately 100 years, the value of EEG has evolved from
a little accepted innovation to a vital procedure for monitoring critically ill
patients. Though its origins were in the study of cognitive neurology, its value in
epilepsy and seizures was quickly realized. Now, in addition to remaining an
essential tool in the diagnosis of epilepsy, EEG is used for the assessment and
prognostication of many different neurological conditions. With newer tech-
niques in data analysis and interpretation, EEG promises to remain vital to the
management of neurologically ill patients.
References
1. Berger H. Über das Elektrenkephalogramm des Menschen. Arch Psychiatr Nervenkr.
1929;87:527–80.
2. Kornmüller AE. Der Mechanismus des Epileptischen Anfalles auf Grund Bioelektrischer
Untersuchungen am Zentralen Nervensystem. Fortschr Neurol Psychiatr. 1935;7:391–400.
3. Fisher MH, Lowenbach H. Aktionsstrome des Zentralnervensystems unter der Einwirkung
von Krampfgiften, 1. Mitteilung Strychnin und Pikrotoxin. Arch F Exp Pathol und Pharmakol.
1934;174:357–82.
4. Kadobayashi I, Nakamura M, Kato N. Changes in visual evoked potentials of schizophrenics
after addition test. Electroencephalogr Clin Neurophysiol. 1977;43:837–45.
5. Poole EW, Chartres J, Wittrick EK. Evoked cerebral sensory responses in the assessment of
surviving function in cerebral disaster. Electroencephalogr Clin Neurophysiol. 1970;29:105.
6. Sutter R, Stevens RD, Kaplan PW. Continuous electroencephalographic monitoring in criti-
cally ill patients: indications, limitations, and strategies. Crit Care Med. 2013;41:1124–32.
7. Oddo M, Carrera E, Claassen J, Mayer SA, Hirsch LJ. Continuous electroencephalography in
the medical intensive care unit. Crit Care Med. 2009;37:2051–6.
8. Sutter R, Fuhr P, Grize L, Marsch S, Rüegg S. Continuous video-EEG monitoring increases
detection rate of nonconvulsive status epilepticus in the ICU. Epilepsia. 2011;52:453–7.
9. Sutter R, Kaplan PW, Rüegg S. Outcome predictors for status epilepticus—what really counts.
Nat Rev Neurol. 2013;9:525–34.
12 R. Sutter and P.W. Kaplan
10. Young GB, Jordan KG, Doig GS. An assessment of nonconvulsive seizures in the intensive
care unit using continuous EEG monitoring: an investigation of variables associated with mor-
tality. Neurology. 1996;47:83–9.
11. Sutter R, Kaplan PW. Uncovering clinical and radiological associations of triphasic waves in
acute encephalopathy: a case-control study. Eur J Neurol. 2014;21:660–6.
12. Sutter R, Stevens RD, Kaplan PW. Clinical and imaging correlates of EEG patterns in hospital-
ized patients with encephalopathy. J Neurol. 2013;260:1087–98.
13. Sutter R, Barnes B, Leyva A, Kaplan PW, Geocadin RG. Electroencephalographic sleep ele-
ments and outcome in acute encephalopathic patients: a 4-year cohort study. Eur J Neurol.
2014;21:1268–75.
14. Stevens RD, Sutter R. Prognosis in severe brain injury. Crit Care Med. 2013;41:1104–23.
15. Oddo M, Rossetti AO. Early multimodal outcome prediction after cardiac arrest in patients
treated with hypothermia. Crit Care Med. 2014;42:1340–7.
16. Gavvala J, Abend N, LaRoche S, et al. Continuous EEG monitoring: a survey of neurophysi-
ologists and neurointensivists. Epilepsia. 2014;55(11):1864–71.
Epidemiology of Seizures
in Critically Ill Adults 2
Jennifer M. Pritchard and Jennifer L. Hopp
Contents
Introduction................................................................................................................................ 13
Status Epilepticus: Overview..................................................................................................... 14
Convulsive Status Epilepticus.................................................................................................... 14
Generalized Convulsive Status Epilepticus....................................................................... 15
Focal Motor Status Epilepticus......................................................................................... 15
Myoclonic Status Epilepticus........................................................................................... 16
Nonconvulsive Status Epilepticus.............................................................................................. 16
Etiology .................................................................................................................................... 18
Preexisting Epilepsy.......................................................................................................... 20
Acute Cerebrovascular Injuries......................................................................................... 20
Traumatic Brain Injury...................................................................................................... 21
Central Nervous System Infections................................................................................... 22
Toxic-Metabolic Disorders and Drug-Related Causes...................................................... 22
Sepsis ............................................................................................................................... 23
Inflammatory and Immune-mediated Disorders............................................................... 24
Hypoxia-Anoxia and Cardiac Arrest................................................................................ 24
Conclusions................................................................................................................................ 25
References.................................................................................................................................. 25
Introduction
Seizures and status epilepticus (SE) are relatively common in critically ill adults, and
manifestations may include convulsive status epilepticus (CSE), nonconvulsive status
epilepticus (NCSE), and nonconvulsive seizures (NCS). Convulsive seizures that do
not meet criteria for status are also seen in this patient population. SE is associated
with significant morbidity and mortality and should be diagnosed and treated appro-
priately. Some challenges in diagnosis and treatment center on the entity of NCSE. This
group is now thought to be a heterogeneous patient population including different
conditions and associated etiologies. In fact, the underlying etiology of seizures and
status is felt to be a very important determinant of overall prognosis and outcome in
this group of critically ill adult patients. In this chapter, the epidemiology, clinical
features, and etiologies of the various SE types will be presented.
The term CSE is often used interchangeably with GCSE. CSE classically refers to
SE with a predominant motor manifestation; when this is in the form of generalized
convulsive seizures, it is best characterized as generalized CSE (GCSE). There are
several other subtypes including focal motor SE and myoclonic SE (MSE).
2 Epidemiology of Seizures in Critically Ill Adults 15
Epidemiology
GCSE is one of the major categories of SE, and it remains a significant problem
with regard to morbidity and mortality in adults. This is despite the fact that the defi-
nition of GCSE has changed over time to be defined as 5 minutes of convulsive
seizures or recurrent seizures over this time period without return to baseline level
of consciousness. The incidence of GCSE can sometimes be difficult to parse out
from the rates of SE in general as many population-based studies include both
GCSE and NCSE. Other inclusion criteria including age groups, definitions of SE,
and other factors may differ, making the data somewhat variable.
GCSE accounts for the majority of cases of SE in most studies, and NCSE may
account for only about 6 % [5]. The incidence of GCSE is age related, with highest
rates in children under one year of age and adults over 60 years of age [5, 6]. A more
detailed discussion of SE in children will be provided in another chapter.
Clinical Features
GCSE is typically characterized by impaired consciousness as well as motor mani-
festations. It typically includes bilateral tonic stiffening followed by clonic (rhyth-
mic jerking) of the limbs, and clinical features may include focal neurologic
findings, such as hemiparesis, in the postictal period. Although GCSE includes both
primary and secondarily generalized seizures, this differentiation may be difficult to
discern in the critically ill adult. EEG can be useful in this classification, but the
semiology can be quite similar, particularly if the clinical onset is not observed or if
seizure and epilepsy history is not known. Asymmetric shaking and unilateral
delayed cessation of clonic activity can be signs of focal onset, but this is not always
a specific finding. Myoclonus prior to generalized tonic-clonic activity may suggest
primary generalized epilepsy, but this can be challenging to gather from witness
reports or even from direct observation.
Epidemiology
The incidence of focal motor SE that does not secondarily generalize may be difficult
to assess in the critically ill patient. CSE with focal onset may be common and inci-
dence is typically included in the incidence of GCSE or NCSE in most population-
based studies. Epilepsia partialis continua (EPC), described below, may be more
commonly seen in children than in the adult population of critically ill patients.
Clinical Features
Focal motor SE can vary greatly in terms of semiology and presentation that is
largely referable to the area of epileptogenic onset. Many cases of generalized SE
are actually focal in onset, but the signs may either not be recognized by observers
or reported by patients, particularly in critically ill adults in an intensive care unit
(ICU) setting. Focal motor SE with preserved consciousness may be the easiest to
16 J.M. Pritchard and J.L. Hopp
recognize as it presents with jerking or clonus of the limb or face, which may spread
to involve other areas. A refractory type of focal motor SE is EPC. This is character-
ized by repetitive focal jerking of typically one part of the body. It usually does not
spread as with the “Jacksonian march” seen in other focal motor SE or secondarily
generalized SE and may have a slower frequency than other focal motor SE types.
Other “non-motor” types of focal SE are nonconvulsive and will be discussed below
in the section on NCSE. These can be quite difficult to identify and classify in a
critically ill patient with altered consciousness.
Epidemiology
MSE is characterized by frequent myoclonic jerks that are typically generalized but
can be focal and may be rhythmic or arrhythmic. This is a large group of heteroge-
neous disorders. In those associated with epilepsy syndromes, myoclonus may be a
characteristic finding, such as juvenile myoclonic epilepsy (JME) or part of a broad
variety of dysfunction (Lennox-Gastaut syndrome, LGS). MSE in these patient
populations is less common than GCSE and may also have a more benign prognosis
than secondary forms. It may also be associated with other neurologic or systemic
dysfunctions that will be discussed later in this chapter, including hypoxia-anoxia.
Clinical Features
Characteristic findings in MSE include frequent myoclonus that is often generalized
but may also be focal. The jerking movements may be rhythmic or arrhythmic, and
often there are characteristic EEG findings which will be discussed elsewhere. MSE
that is epileptic in origin may be seen with other GCSE (as in JME) as well as other
seizure types such as atonic or myoclonic-astatic seizures in LGS. These typically
can be relatively easily distinguished from other forms of persistent myoclonus and
MSE by history. While the former have a history of epilepsy, other nonepileptic
types, sometimes termed “status myoclonus,” are associated with an underlying dif-
fuse etiology such as anoxia or other forms of encephalopathy. When seen in the
setting of other medical conditions, the myoclonus is often nonrhythmic, prolonged,
and continuous, with large amplitude jerking movements. These are classically
described involving the face, trunk, and limbs, but may also be multifocal.
recordings. Some studies suggest that NCSE typically is diagnosed in the first hour,
while others do not. Although SE has historically been easier to recognize by semi-
ology with repeated or prolonged convulsions, recognition of NCSE followed later.
In the early nineteenth century, some episodes of prolonged confusional states were
thought to be due to seizures, but it was not until EEG was introduced in the 1940s
that NCSE was conclusively established as a valid entity [13–15]. In 1956, Gastaut
used the term “psychomotor status” to describe another type of NCSE associated
with altered mental status [13]. In 1962, an international symposium codified SE by
characterizing it as a term for a repeated or prolonged seizure as to create a fixed and
lasting epileptic condition for at least 30–60 min [15, 16]. The same group also
promoted the view that there were many types of SE.
There are several ways to think about categorization of NCSE, and the definition
of the term remains controversial. The narrowest definition of the term refers only
to two categories. They include absence (previously petit mal) status and focal or
complex partial SE (previously psychomotor SE) [2, 11, 17, 18]. With wider use of
EEG and cEEG monitoring, the stratification of this term has evolved.
Over time, other subtypes and classifications have been proposed, with the con-
cept that there may be as many types of NCSE as there are seizure types or classifi-
cations. There are a variety of accepted definitions of NCSE, but in addition to a
change in mental status, there is a common working definition that is often used for
EEG criteria that also includes a “significant improvement in clinical state or base-
line EEG after antiepileptic drug” [19]. These criteria can be problematic, however,
in that one of the criteria establishes the definition by responsiveness to anticonvul-
sant treatment, which is not always the case in resistant NCSE [20].
Although semiology can be broadly divided between CSE and NCSE as those
forms of status with or without convulsions, there may be more subtle features of
partial or focal status that are increasingly recognized. Typically, the lack of major
motor manifestations delineates the difference between CSE and NCSE, but many
patients with NCSE have minor abnormal motor findings. These may include nystag-
mus, facial twitching, or tonic eye movements [18]. As might be expected, the find-
ings typically correspond to the origin of onset of the localization-related epilepsy.
While on one hand findings in temporal lobe NCSE may be characterized as
confusion, parietal lobe NCSE, which is much less common, may be manifest by
findings referable to the areas involved. The most common types of parietal lobe
seizures arise from the postcentral gyrus and are typically described as a positive or
negative sensation. Patients describe sensations in NCSE as prolonged paresthesias,
pain, sexual phenomenology, or a widespread body “aura” [21]. Pain and percep-
tions of heat or cold are less common, as are seizures with sexual phenomenology
or psychiatric phenomena, or disturbances of body image, but they have also been
associated with seizures of parietal lobe origin and also those of parietal
NCSE. Prolonged ictal sensory changes are thought to be rare and are uncommonly
reported. Recognition of somatosensory SE requires that patients report symptoms
and this may be hindered when patients are amnestic for the auras or sensory symp-
toms during the seizure or if the area of ictal onset has spread to lead to confusion,
thus impairing patient report.
18 J.M. Pritchard and J.L. Hopp
It is more common for these patients to have had a witnessed seizure or GCSE,
but it is notable that there is a large portion of critically ill patients who may not
have had a clinically evident seizure. The diagnosis can be difficult, particularly as
patients in the ICU setting may be thought to be postictal after clinically evident
seizures. It has also, and still is, often mistaken for other reasons for change in men-
tal status [22].
There are several ways to think about NCSE, and it is useful to understand that
the categories and divisions that are utilized are not mutually exclusive. NCSE has
been divided into different types by semiology, EEG patterns, and association with
varied levels of consciousness. Traditionally, NCSE was thought to primarily be
associated only with epilepsy syndromes, as in the “wandering confused” patient
with epilepsy who has a relatively good prognosis, now other presentations are rec-
ognized. These are often seen in the critical care setting and are seen in acutely ill
patients with impaired mental status. Motor manifestations may or may not be seen.
Clinicians should be attuned to the possibility of NCSE, even in patients without
clinically evident seizures, although NCSE that follows uncontrolled SE is the more
common presentation.
By EEG criteria, NCSE is typically categorized as generalized or lateralized. There
are often blurred lines in patients with altered consciousness or coma who have peri-
odic or continuous patterns on EEG that may resemble those typical in NCSE patients.
It is not yet fully clear whether treating these patterns may improve outcome or is then
diagnostic of NCSE. Some groups advocate categorizing NCSE into “NCSE proper”
and “comatose NCSE” to delineate these patient populations [23].
Etiology
Among critically ill adults, causes of seizures and SE are diverse, and this contrib-
utes to the notion that not all such patients can be approached in the same manner.
Furthermore, the underlying etiology of seizures and SE has increasingly been rec-
ognized as a critical determinant of prognosis and outcome in this patient popula-
tion. Thus, prompt recognition of the root cause(s) of seizures and SE, along with
its subsequent evaluation and treatment, is crucial.
In critically ill adults, etiologies are varied. Important causes of acute seizures
and SE include insufficient dosages or low levels of antiepileptic drugs (AEDs) in
patients with known epilepsy, cerebrovascular disorders, traumatic brain injury
(TBI), hypoxia-anoxia, and infectious etiologies including sepsis, brain tumors, and
toxic-metabolic disorders [24, 25]. Less common, but also important, etiologies
including inflammatory and immune-mediated conditions are garnering increasing
interest. Such disorders include paraneoplastic syndromes and autoimmune enceph-
alitides such as anti-N-methyl-d-aspartate (NMDA) receptor encephalitis. Many of
these important causes will be discussed individually in greater detail in the sections
that follow. Given the broad spectrum of associated underlying conditions, critically
ill patients with seizures and SE are, in many ways, a very heterogeneous group
(Table 1).
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CHAPTER I.
Spiraculis solitariis.
Lophius.
Acipenser.
Cyclopterus.
Balistes.
Ostracion.
Tetrodon.
Diodon.
Centriscus.
Syngnathus.
Pegasus.
Pisces Apodes.
Muræna.
Gymnotus.
Trichiurus.
Anarhichas.
Ammodytes.
Ophidium.
Stromateus.
Xiphias.
Pisces Jugulares.
Callionymus.
Uranoscopus.
Trachinus.
Gadus.
Blennius.
Pisces Thoracici.
Cepola.
Echeneis.
Coryphæna.
Gobius.
Cottus.
Scorpæna.
Zeus.
Pleuronectes.
Chæetodon.
Sparus.
Labrus.
Sciæna.
Perca.
Gasterosteus.
Scomber.
Mullus.
Trigla.
Pisces Abdominales.
Cobitis.
Amia.
Silurus.
Teuthis.
Loricaria.
Salmo.
Fistularia.
Esox.
Elops.
Argentina.
Atherina.
Mugil.
Mormyrus.
Exocœtus.
Polynemus.
Clupea.
Cyprinus.
b. Malacoptérygiens.
Abdominaux.
Cyprinoïdes.
Siluroïdes.
Salmonoïdes.
Clupeoïdes.
Lucioïdes.
Subbrachiens.
Sparoïdes.
Pleuronectes.
Discoboles.
Apodes.
Murenoïdes.
B. Cartilagineux ou Chondroptérygiens.
Sturioniens.
Plagiostomes.
Cyclostomes.