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HEALTH AND WELLNESS 1/2013
HEALTH AND WELLNESS
CHAPTER VII
Department of Neurology, Medical University of Lublin, Poland
Katedra i Klinika Neurologii, Uniwersytet Medyczny w Lublinie
MAGDALENA GODEK, ANNA SOJKA, MAŁGORZATA CHLEBICKA,
EWA PAPUĆ, MARTA TYNECKA-TUROWSKA, KONRAD REJDAK
Repetitive seizures and status epilepticus – clinical presentation
and prognosis based on prospective analysis of patients
Napady gromadne i stan padaczkowy – obraz kliniczny i rokowanie
w oparciu o prospektywną analizę pacjentów
INTRODUCTION
Repetitive seizures (RS) and status epilepticus (SE) are associated with increased
risk of mortality and requires proper management in pre-hospital and hospital setting
[1]. Identification of outcome-predictive factors could lower the risk of serious complications. Recently, a prognostic score STESS (Status Epilepticus Severity Score)
was proposed to predict mortality in status epilepticus using four variables available
at presentation [6, 8]. Epilepsy is the most common serious neurological disorder,
affecting approximately 1 in 150 people, and status epilepticus (SE) is sometimes
described as the maximal expression of epilepsy, being associated with both shortand long-term significant mortality and morbidity. There are almost as many types
of status as there are of seizures. SE describes a unique pathological state, during
which seizures tend to become self-perpetuating. The definition of SE was evolving
and still there is no general consensus how to describe this pathological condition.
Different time of duration was used: 30 min in the guidelines of the Epilepsy Foundation of America’s Working Group on Status Epilepticus, 20 min and 10 min in the
VA Cooperative Trial. Additionally, the operational definition of SE was proposed
with 5 min of seizures in order to emphasize the need of early treatment. Early therapeutic intervention diminishes the risk of SE-induced neuronal injury and of the
time-dependent development of pharmacoresistance. Our current understanding of
the basic mechanisms of SE in animal models and in clinical situations is in accordance with the Clark’s description of three phases of SE [1].
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Impending status epilepticus is defined as continuous seizures or intermittent
seizures without full recovery of consciousness between seizures lasting more than 5
minutes. Established status epilepticus is defined as clinical or electrographic seizures lasting more than 30 min without full recovery of consciousness between seizures. The transformation from impending SE to established SE is probably a continuum, but there is good support in the clinical and experimental literature for a cutoff at 30 min: this is the time constant of transformation from prolonged seizure to
SE. This also corresponds with the results of experimental studies when SE become
self-sustained in animals, when SE-induced damage becomes evident, and when
pharmacoresistance to anticonvulsants may develop. The term subtle status epilepticus was coined by Treiman to describe the late, burned-out stage of SE during which
both the motor and electroencephalographic (EEG) expression of seizures becomes
less evident. In most electrical and chemical models of SE initiated in conscious,
unanesthetized animals, seizures rapidly become self-sustaining despite the withdrawal of the epileptogenic stimulus. Human data are far less clear, but show that
seizures which last more than 30 min rarely stop spontaneously. Cerebral metabolic
demand is generally sustained during phase 1 tonic-clonic status, but not during
phase 2, which is accompanied by profound metabolic complications. The combination of metabolic decompensation and the direct neurotoxic effects of ongoing seizure activity contribute to an association between long duration of status and poor
outcome [1].
Experimental data show that after 30 min of intermittent stimulation of an excitatory glutamatergic pathway in the rat, stopping the stimulation no longer stops electrographic or behavioral seizures, which self-perpetuate for many hours and eventually become subtle. It was showed that these properties are shared by many others
excitatory pathways [9].
The aim of the study was to prospectively analyze a cohort of patients presenting
with repetitive seizures and status epilepticus at the Emergency Department in order
to identify the risk factors correlating with the outcome. In addition, STESS was
applied to determine its utility in the early assessment of patients.
MATERIALS AND METHODS
SE was defined as ongoing seizures, or repetitive seizures without intercurrent
normalization of consciousness or return to baseline, for at least 30 minutes. RS
were defined as recurrent seizures with intervals of returning to full consciousness.
The study group consisted of 50 subjects fulfilling the criteria of RS (n=27) or EEG
confirmed SE (n=23). Outcome at discharge (mortality, return to baseline clinical
conditions) was analyzed in relation to demographics, clinical features, and aetiology. Aetiologies were also classified based on whether or not they were potentially
fatal independently of SE. In addition to demographic characteristics, we identified
previous history of seizures, seizure semiology focusing on the worst manifestation
before treatment (in descending order of gravity: nonconvulsive SE in coma, generalized convulsive, complex partial, myoclonic or absence or simple partial), time
between seizure onset and institution of the first specific treatment (dichotomized as
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Magdalena Godek, Anna Sojka, Małgorzata Chlebicka, Ewa Papuć,
Marta Tynecka-Turowska, Konrad Rejdak
Repetitive seizures and status epilepticus – clinical presentation
and prognosis based on prospective analysis of patients
< or ≥ 1 h), and SE etiology, classified as acute symptomatic, remote symptomatic,
progressive symptomatic, and idiopathic/cryptogenic).
RESULTS
 The study group consisted of 42% of females and 58% of males with median age
of 53 (18-86) years.
 The most frequent risk factors of RS and SE were: alcohol related (40%), acute
craniocerebral insult (22%), epilepsy related (10%) while the cause was undetermined in 18% of cases.
 Repetitive seizures were associated with good prognosis and return to baseline
clinical condition in 100% of cases.
 Similarly, in those cases where RS transformed into SE (n=8), the outcome was
favorable. In the total SE subgroup (n=23) the mortality rate was 10% and death
was associated with age>or=65 (p=0.02) and coma or stupor at presentation
(p=0.01).
 STEES score of 6 significantly correlated with fatal outcome (p<0,001).
 There were no significant differences in the course of disease determined according to gender, SE type, history of epilepsy, or time to treatment.
DISCUSSION
The current study clearly demonstrates that the early identification of patients at
risk of mortality is crucial for proper management. We provide the external validation of the STEES and confirm that the scale is an important instrument with relevant prognostic value for patients suffering SE [6, 8].
Repeated seizures produce complex cascades of pathophysiological and biochemical changes in the brain [1]. The first milliseconds to seconds are dominated
by the release of neurotransmitters and modulators, the activation and inactivation of
ion channels, and receptor phosphorylation and desensitization. Within seconds to
minutes, receptor trafficking, mainly of the GABA and glutamate receptors, is responsible for the key adaptations. The existing receptors can move from the synaptic
membrane into endosomes, or be mobilized from storage sites to the synaptic membrane. This process enhances excitability by decreasing the number of inhibitory
receptors and increasing the number of excitatory receptors in the synaptic cleft. In
the minutes to hours, neuropeptide modulators often increase the expression of proconvulsive neuropeptides and decrease the availability of inhibitory neuropeptides,
and this maintains enhanced excitability. Finally, in the hours to perhaps days to
weeks following seizures, long term changes in gene expression occur. The changes
in gene expression are the combined effects of repeated seizures, of seizure-induced
neuronal death, and of the subsequent neuronal reorganization. Some of the gene
expression represents plastic adaptation to seizure activity. In addition to significant
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case fatality, status (particularly tonic-clonic status) is associated with considerable
morbidity, in terms of cognitive and neurological deficit.
There is general consensus that status epilepticus has deleterious effects on brain
tissue, but whether brief recurrent seizures are also destructive to neurons is discussed controversial. The epilepsies form a heterogeneous group of conditions in
which overt seizures are only one manifestation. Apparently similar seizure may
cause cerebral damage in the context of one form of epilepsy but not in another.
Subclinical seizures and interictal epileptiform activity might also cause cerebral
damage. Some medications might increase or decrease the risk for secondary neuron
injury. In addition, genetic factors may predispose some individuals to be at greater
risk than others. Currently available methods to assess the degree of progression of
neurodegeneration in epilepsy patients include neuropsychological assessment, neuroimmaging or pathological studies of resected in vivo or postmortem brain tissue
[7].
Pathological studies
Severe hippocampal neuron loss is associated with a long history of epilepsy and
secondarily generalized seizures. These studies have implied that damage develops
over many years and is in part programmed cell death (apoptosis). The density and
branching of dendritic spines are reduced. Sprouting of mossy fibers can be seen in
the dentate gyrus in resected hippocampi. Increased expression of polysialylated
neural cell adhesion molecule (PSANCAM) indicates axonal growth and plasticity
in the dentate gyrus and the CA1 region of hippocampi and whether there is neurogenesis in sclerotic hippocampi. Astrocytosis is commonly found in resected tissue.
The presence of activated microglia suggests continuing injury, and increases in the
CA1 and CA3 subregions of resected hippocampi imply a continuing process of
damage. There are much fewer data on the effects and consequences of epileptic
seizures and the epilepsies on the neocortex and cerebellum. The well-known association of cerebellar atrophy with chronic epilepsy has often been also described.
The available evidence suggests that chronic epilepsy and recurrent seizures are
associated with neuronal injury and reactive changes in human hippocampi. The
direct access to human cells in the CNS under in vivo conditions is not feasible and
therefore, surrogate markers have to be used [1].
MRI studies
Numerous studies provided evidence of the progressive atrophy of the mesial
part of the temporal lobe and hippocampus in the course of the refractory epilepsy.
However, it is much more difficult to reliably demonstrate extrahippocampal structural changes in long term prospective studies. It was reported that overt structural
cerebral damage was not an inevitable consequence of epileptic seizures. In general,
brain volume reduction in epilepsy was the cumulative effect of an initial precipitating injury and age-related cerebral atrophy. Significant atrophy developed in individual patients, particularly those with temporal lobe and generalized epilepsy.
Longer periods of observation are required in order to detect more subtle effects of
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Magdalena Godek, Anna Sojka, Małgorzata Chlebicka, Ewa Papuć,
Marta Tynecka-Turowska, Konrad Rejdak
Repetitive seizures and status epilepticus – clinical presentation
and prognosis based on prospective analysis of patients
seizures. Nevertheless, in vivo imaging studies have the remain a standard to identify and quantify secondary cerebral damage caused by epilepsy before there is any
clinical accompaniment, and to act as a surrogate end point for intervention and
preventative strategies. Structural MRI, however, may be insensitive to relatively
subtle neuron loss and injury. MR spectroscopy (MRS) allows the evaluation of both
the integrity and function of neurons by measuring N-acetyl aspartate (NAA), a
normal byproduct of neuronal cellular metabolism. NAA is a marker of neuron cell
dysfunction, not merely of volume loss. Abnormalities of metabolite profiles may be
found in temporal lobes with normal MRI and bilateral abnormalities have been
noted in up to 50% of patients with apparently unilateral structural abnormality,
indicating that MRS may be more sensitive for detecting pathology.
The sensitivity of MRS to abnormality may be greater than that of MRI, but
changes are nonspecific and the test–retest coefficient of reliability for the measurement of NAA using MRS is approximately 15–20%. The reliability is poorer for
other metabolites. MR spectroscopy has shown elevation of lactate during and for a
few hours after complex partial seizures and NAA decreases after episodes of status
epilepticus. This method is potentially useful to assess the acute effects of seizures
on neuron function but detailed studies correlating MRS changes with other biochemical and metabolic parameters are needed in order to increase its specificity for
seizure induced pathological phenomena [3].
Body fluid biomarkers
There is an increasing interest in biochemical brain-specific surrogate markers
sensitive enough to detect the subtle pathological processes induced by seizures
under in vivo conditions. CSF examination provides an unique opportunity to get
more insight into the pathophysiology of potential brain damage under in vivo conditions.
There were many attempts to find such markers published in the scientific literature. Among the most extensively studied were neuron-specific enolase (NSE) and
S100B protein demonstrated to be raised in CSF and serum of patients recovering
from status epilepticus or recurrent seizures. However, the results differed from
study to study depending on the population characteristics and especially seizure
type. This may at least in part be related to the fact that NSE and S100B are of limited cellular specificity [4].
Thus, there is still need for searching more highly specific and sensitive biomarkers for detecting in vivo damage to neurons following seizures.
Brain specific proteins measured in CSF or serum are of high importance as indicators of brain cell activity or damage. Among them, the neuron specific enolase,
neurofilament heavy chain protein (NfH) and orexin-A (hypoceretin-1) were proven
to be sensitive and specific markers of neuron pathology, while S100B and glial
fibrillary acidic protein (GFAP) are reliable markers of glial activation/damage.
Neurofilaments (Nf), represent a group of proteins specifically expressed in neurons and axons and have emerged as promising biomarkers for neurodegeneration
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experimentally and clinically in a range of neurological disorders. The neurofilament heavy chain (NfH) is the most extensively phosphorylated protein of the human body with regulatory influences on cell structure homeostasis and axonal
transport and is released into the CSF following axonal damage, predominantly in
acute neurological diseases. So far the effects of seizures on Nf content in body
fluids as markers of neuronal damage has not been studied [4].
The two related peptides (Orexin-A and B, or hypocretin-1 and -2) are produced
by a very small population of cells in the lateral and posterior hypothalamus by
cleavage of a single precursor protein. Discovery of these novel hypothalamic neuropeptides led to extensive research on their physiological functions. Initially the
orexin/hypocretin system was thought to be primarily involved in the stimulation of
food intake, but its deficiency has soon been found in animal and human narcolepsy.
Secondary impairment in the hypocretin neurotransmission, probably due to direct
or indirect damage of the posterior hypothalamus and its connections, has also been
reported in some neurological conditions manifesting with excessive somnolence.
Prolonged or recurrent convulsive seizures, as well as self sustained status epilepticus, is medical emergency with a complex pathophysiology associated with various
physiological and biochemical changes and neuronal damage. In particular, changes
in brain expression and cerebrospinal fluid concentration of various neuropeptides
were described. In a pilot study we reported the decreased levels of orexin-A in CSF
of patients suffering from repetitive seizures what indicated that impairment of orexin system might be a part of the seizure related pathophysiology. Further studies are
needed in order to assess the value of this biomarker in wide range of clinical and
experimental conditions related to episodes of seizures and status epilepticus [5].
Cerebrospinal fluid (CSF) total tau (T-tau) and phosphorylated tau (P-tau) measurements have been suggested for the diagnosis of Alzheimer's disease, and T-tau
may also be a marker of axonal damage and neuronal degeneration in a range of
other neurologic diseases. One recent study examined the effects of seizures on tau
levels in CSF of epileptic patients. Epileptic seizures with unknown etiology did not
increase CSF tau levels. Abnormal tau levels were associated with either acute or
remote symptomatic seizures with known etiology. The presence of elevated CSF
tau increases the probability of symptomatic cause in a patient with a seizure.
The markers with the potential specificity for endogenous neuroprotection include: kynurenic acid, heat shock proteins: 27, 70. Kynurenic acid (KYNA), an
intermediate metabolite of L-kynurenine is a broad-spectrum excitatory amino acid
antagonist and possesses neuroprotective activity. Those metabolites are sensitive
markers of peripheral macrophage and CNS residual microglia activation. Interestingly, it was demonstrated that human astrocytes may also produce kynurenic acid
but not the neurotoxic metabolites 3-hydroxykynurenine and quinolinic acid due to
the lack of kynurenine hydroxylase.
Only few studies examined the effects of several classic convulsants (pentylenetetrazole, pilocarpine, bicuculline, or kainic acid) on the extracellular concentrations
of the KYNA in the rat brain. In all seizure paradigms, KYNA levels in the dialysate
began to rise within 1 h and gradually reached a plateau approximately 4 h after
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Magdalena Godek, Anna Sojka, Małgorzata Chlebicka, Ewa Papuć,
Marta Tynecka-Turowska, Konrad Rejdak
Repetitive seizures and status epilepticus – clinical presentation
and prognosis based on prospective analysis of patients
administration of the convulsants. Peak increases were 1.5-3-fold over basal levels.
The duration of the elevation in KYNA levels was significantly prolonged following
kainic acid application. In the kainic acid model, extracellular KYNA was also
measured and found to be increased in the ventral hippocampus, piriform cortex, and
striatum. There are no studies measuring KYNA levels in CSF of epileptic patients,
what might be important of assess the activation of endogenous protection after
seizure activity.
Similarly, there has been a long interest in studying the relationship between heat
shock proteins (HSP) expression and the evidence of neuronal damage in the most
susceptible brain areas after seizures. Their increased expression was repeatedly
demonstrated in several animal models upon induction of acute seizures or other
types of brain insults confirming their value as markers of stress and damage but
their effective cytoprotective role is still speculative. However, all previous studies
were experimental or based on post-mortem or resected material from epileptic
patients. It is very important to study the mechanisms of endogenous neuroprotection as the imbalance between neurotoxic and neuroprotective mechanisms may
determine the final outcome in brain structures after the seizures, with potential
consequences for the neurological status of patients [4].
The mechanism, which may link and mediate both neuroprotection and neurodegeneration is the inflammatory process, which is increasingly recognized as an
important component of the epilepsy pathogenesis. Proinflammatory and antiinflammatory cytokines and related molecules have been described in CNS and
plasma, in experimental models of seizures and in clinical cases of epilepsy. Inflammation involves both the innate and the adaptive immune systems and shares
molecules and pathways also activated by systemic infection. Experimental studies
in rodents show that inflammatory reactions in the brain can enhance neuronal excitability, impair cell survival, and increase the permeability of the blood-brain barrier
to blood-borne molecules and cells. Moreover, some antiinflammatory treatments
reduce seizures in experimental models and, in some instances, in clinical cases of
epilepsy. However, inflammatory reactions in brain also can be beneficial, depending on the tissue microenvironment, the inflammatory mediators produced in injured
tissue, the functional status of the target cells, and the length of time the tissue is
exposed to inflammation.
In particular, the nitrosative stress might be very important in that context as
there are experimental studies demonstrating the effects of seizures on generation of
the free radicals and neurotoxic nitrosative end products. However, there are only
few studies addressing that issue in human subjects with epilepsy. The production of
the nitric oxide metabolites: nitrate/nitrite in body fluids of epileptic patients as well
as in experimental animals subjected to models of status epilepticus in relation to
other biomarkers of neuronal damage or endogenous protection [1].
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Management
The inappropriate treatment of non-epileptic seizures carries a significant risk of
iatrogenic complications, including respiratory failure or arrest and admission to
ITU [2]. However, delayed treatment of tonic-clonic status can be equally dangerous. Lorazepam is the drug of choice among the first line drugs, in all current guidelines (Royal College of Physicians Edinburgh 2003; Scottish Intercollegiate Guidelines Network 2003; NICE 2004). Intravenous diazepam has been used traditionally,
and although it has a rapid onset of action, it is quickly redistributed into fatty tissue
often leading to rebound seizures. If benzodiazepines fail, currently approved treatment for established status include: phenytoin, phenobarbitone and fosphenytoin.
Intravenous valproate is an important option among II line drugs, and has been
shown to be safe and effective. When it comes to refractory status, expert consensus
and all current guidelines advise that if treatment is still not controlling seizures at
this stage (between 30 and 60 min), the patient should be transferred to ITU for
general anaesthesia, both to suppress seizures and for the management of the systemic adverse effects of the epilepsy and the drugs being used to suppress it. Three
agents are in common use at present: thiopentone, propofol and midazolam. If seizures recur, the diagnosis should be revisited, both in terms of whether this is truly
epilepsy (necessitating EEG in the unconscious patient), and with respect to aetiology. Even in patients with known epilepsy, magnetic resonance imaging, and cerebrospinal fluid (CSF) examination, should be undertaken or repeated to exclude new
pathology.
REFERENCES
1. Chen JW, Wasterlain CG. Status epilepticus: pathophysiology and management
in adults. Lancet Neurol. 2006 Mar;5 (3): 246-56.
2. Lasoń W, Dudra-Jastrzębska M, Rejdak K, Czuczwar SJ. Basic mechanisms of
antiepileptic drugs and their pharmacokinetic/pharmacodynamic interactions: an
update. Pharmacol Rep. 2011; 63 (2): 271-92.
3. Logroscino G., Hesdorffer D.C., Cascino G., Hauser A. (2008) Status Epilepticus Without an Underlying Cause and Risk of Death. Arch Neurol/ vol. 65:221224.
4. Rejdak K, Kuhle J, Rüegg S, Lindberg RL, Petzold A, Sulejczak D, Papuc E,
Rejdak R, Stelmasiak Z, Grieb P. Neurofilament heavy chain and heat shock protein 70 as markers of seizure-related brain injury. Epilepsia. 2012 May;53
(5):922-7.
5. Rejdak K, Papuć E, Grieb P, Stelmasiak Z. Decreased cerebrospinal fluid
hypocretin-1 (orexin A) in patients after repetitive generalized tonic-clonic seizures. Epilepsia. 2009 Jun;50 (6):1641-4.
6. Rossetti A.O., Hurwitz S., Logroscino G., Bromfield E.B. (2006) Prognosis of
status epilepticus: role of aetiology, age, and consciousness impairment at
presentation. J Neurol Neurosurg Psychiatry 77:611-615.
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Magdalena Godek, Anna Sojka, Małgorzata Chlebicka, Ewa Papuć,
Marta Tynecka-Turowska, Konrad Rejdak
Repetitive seizures and status epilepticus – clinical presentation
and prognosis based on prospective analysis of patients
7. Rossetti A.O., Logroscino G., Bromfield E.B. (2005) Refractory Status Epilepticus. Effect of Treatment Aggressiveness on Prognosis. Arch Neurol/
vol.62:1698-1702.
8. Rossetti A.O., Logroscino G., Milligan T.A., Michaelides C., Ruffieux Ch.,
Bromfield E.B. (2008) Status Epilepticus Severity Score (STESS). A tool to orient early treatment strategy. Neurology 255:1561-1566.
9. Wasterlain CG, Baldwin R, Naylor DE, Thompson KW, Suchomelova L, Niquet
J. Rational polytherapy in the treatment of acute seizures and status epilepticus.
Epilepsia. 2011 Oct;52 Suppl 8:70-1.
Table 1. Study population characteristics
Characteristics
Total
RS
SE
n
50
27
23
Age, y
53 (18-86) 55 (18-78) 51 (37-86)
Gender (F/M)
21/29
14/13
7/16
Previous seizures
61%
65%
58%
Acute etiology
28%
10%
47%
Comatose
42%
15%
70%
GC SE
93%
95%
90%
Time to treat.<1 h 5.5 (2-11) 5.0 (2-7) 6.0 (4-11)
Figure 1. Clinical outcome in SE patients (n=23)
80
72
Survival
70
Death
Patients (%)
60
50
40
30
20
10
10
10
8
0
2
0
0-2
3
4
5
6
STESS
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ABSTRACT
Recently, a prognostic score STESS (Status Epilepticus Severity Score) was proposed to predict mortality in status epilepticus. The aim of the study was to prospectively analyze a cohort of patients presenting with repetitive seizures (RS) and status
epilepticus (SE) in order to identify the risk factors correlating with the outcome.
The study group consisted of 50 subjects with RS (n=27) or EEG confirmed SE
(n=23). Outcome at discharge (mortality, return to baseline clinical conditions) was
analyzed in relation to demographics, clinical features, and aetiology. The study
group consisted of 42% of females and 58% of males with median age of 53 (23-78)
years. Repetitive seizures were associated good prognosis with return to baseline
clinical condition in 100% of cases. Similarly, in those cases where RS transformed
into SE (n=8), the outcome was favorable. In the total SE subgroup (n=23) the mortality rate was 10% and death was associated with age>or=65 (p=0.02) and coma or
stupor at presentation (p=0.01). STEES score of 6 significantly correlated with fatal
outcome (p<0,001). The STEES scale is an important instrument with relevant
prognostic value for patients suffering SE.
STRESZCZENIE
W ostatnim czasie zaproponowano skalę STESS (skala ciężkości stanu
padaczkowego) dla prognozowania śmiertelności w stanie padaczkowym. Celem
pracy była prospektywna analiza grupy pacjentów z powtarzającymi się drgawkami
(RS) oraz pacjentów w stanie padaczkowym (SE) w celu identyfikacji czynników
ryzyka korelujących z wynikami leczenia. Grupa badana składała się z 50
pacjentów; w tym z RS (n=27) oraz z potwierdzonym przez badanie EEG SE
(n=23). Stan przy wypisie (śmiertelność, powrót do stanu sprzed zachorowania) był
analizowany w korelacji z danymi demograficznymi, objawami klinicznymi oraz
etiologią. Grupa badana składała się w 42% z kobiet i 58% z mężczyzn, ze średnią
wieku 53 (23-78) lata. W 100% przypadków powtarzających się drgawek rokowanie
było dobre. Podobnie w przypadkach, w których powtarzające się drgawki
ewoluowały w stan padaczkowy SE (n=8) wynik leczenia był korzystny. Natomiast
ogółem w podgrupie pacjentów w stanie padaczkowym (n=23) wskaźnik
śmiertelności wynosił 10%, a zgon był powiązany z wiekiem > lub=65 (p=0,02)
oraz śpiączką lub stuporem (p=0,01). Punktacja w skali STEES z wynikiem 6
istotnie korelowała ze zgonem (p<0,001). Skala STEES jest ważnym instrumentem
w istotnej ocenie prognostycznej pacjentów cierpiących na stan padaczkowy.
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