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Nonconvulsive Status Epilepticus and Coma

By Demet Ilhan Algın, Gülgun Uncu, Demet Ozbabalık Adapınar and Oğuz Osman Erdinç

Submitted: May 21st 2019Reviewed: August 29th 2019Published: November 5th 2019

DOI: 10.5772/intechopen.89428

Downloaded: 7

Abstract

Nonconvulsive status epilepticus (NCSE) is common in patients with coma with a prevalence between 5 and 48%. Nonconvulsive status epilepticus (NCSE) is an electroclinical state associated with an altered mental status (AMS) but lacking convulsive motor activity. It is difficult to diagnose in the obtunded/comatose patients. Such patients have often other serious medical conditions, and the diagnosis of NCSE is frequently delayed in these patients. Diagnosing NCSE demands a high degree of clinical suspicion and for that reason likely remains under-recognized. The most important question, however, is whether the treatment of NCSE in coma improves the outcome of these patients or not. In this review, we aimed to summarize the EEG patterns in NCSE to further delineate the borders between comatose forms of NCSE and coma-epileptiform discharges and to evaluate modified EEG criteria for NCSE in a coma.

Keywords

  • coma
  • nonconvulsive status epilepticus (NCSE)
  • EEG
  • periodic discharges
  • consciousness

1. Introduction

Coma is the disorder of consciousness because of the damage to diffused bilateral cerebral hemisphere corte or ascending reticular activation system (ARAS) [1].

This neural network starts from the dorsal part of the upper pons, continues in the mesencephalon, connects to the thalamus and diffuses widely from there to both hemispheres. In addition, ARAS is associated with some nuclei in the pons and mesencephalon, the posterior hypothalamus, and the basal forebrain. Communication in this network is established through neurotransmitters such as acetylcholine, noradrenaline, serotonin and dopamine [2]. Structural or biochemical damage or disruption of this neural network may cause unconsciousness. The most severe picture in the spectrum of consciousness disorders is coma. In a comatose patient, alertness and awareness are completely lost. Many causes of both intracranial and systemic origin can cause coma. In order to begin specific treatment as soon as possible, the underlying cause of the coma should be established as quickly as possible. For this purpose, the patient should be systematically approached and the possible causes of the mechanism should be considered in five major categories [3]:

  1. Unilateral hemispheric mass lesions compressing diencephalon or brain stem.

  2. Bilateral hemispheric lesions affecting the reticular formation and thalamocortical cycle fibers at thalamus level.

  3. Infratentorial lesions that compress or damage the reticular formation in the brain system.

  4. Diffuse lesions affecting the physiological function of the brain.

  5. Psychiatric conditions mimicking coma.

The evaluation of coma patients falls within the responsibility of physicians working in many disciplines. Detecting the cause of the coma requires detailed investigation and deductive effort. The physician should consider the patient as a whole and be able to synthesize the information obtained from history, examination and diagnostic tools and theoretical information.

2. Nonconvulsive status epilepticus

Nonconvulsive status epilepticus (NCSE) which has higher morbidity and mortality is a treatable disorder when diagnosed properly. NCSE has special symptoms such as unexplained confusion or coma or vegetative status and aura which can distinguish from the normal conditions. NCSE is a continuous seizure activity with a minimum duration of 10–30 min on EEG [4]. In previous studies used different EEG criteria to identify the NCSE patients, the prevalence of NCSE ranges from 5 to 48% and the actual prevalence of NCSE is still unknown [5].

The new ILAE classification is based on 4 axes 1 being the semiology (Table 1); axis 2 is the etiology; axis 3 is EEG correlates, and axis 4 is the age of the patient. This concept takes account of the requirements for a classification supporting a clinical diagnosis, enabling research through standardization while ensuring an individualized treatment concept for the patient [6, 7].

Table 1.

New ILAE classification of NCSE axis 1.

Clinical evidence may vary greatly in NCSE. Negative and positive symptoms can be evaluated into two groups. Negative symptoms are anorexia, aphasia/mutism, amnesia, catatonia, coma, lethargy and negative symptoms are agitation, aggression, automatisms, twinkle, crying, delirium, echolalia, laughing, nausea-vomiting, nystagmus-eye deviation, perseveration, anxiety and psychosis [8]. Nonconvulsive status epilepticus is a treatable neurologic emergency when it is diagnosed properly. Diagnostic criteria depend on clinical status, EEG findings and response to treatment. During the initial evaluation, EEG recording is crucial for patients with acute confusion [6].

Although the etiologies of NCSE and coma intersect, NCSE is a distinct clinical picture and an electroclinic condition without convulsive motor activity. Diagnosis is difficult in a comatose patient. The diagnosis of NCSE is often delayed in those patients. Clinically, a high degree of suspicion is required for diagnosis. Ictal-interictal discrimination of activity on EEG is difficult despite the newly defined criteria and these criteria have practical application difficulties. Another important issue is how aggressive treatment of NCSE in comatose patients should be, because the positive or negative effect of NCSE treatment on the prognosis of those patients is not well known. A distinction should be made between patients with coma or other severe disorders and those with really epileptic mechanisms and treatment should be decided accordingly. Specific EEG patterns are not seen in a coma [9].

2.1 EEG patterns in comatose patients

2.1.1 Intermittent rhythmic delta activity

Among EEG findings in encephalopathy, intermittent rhythmic delta activity (IRDA) is considered to lie at the milder end of the spectrum of coma EEG patterns. IRDA may appear in patients who are awake or who are mildly lethargic or stuporous; IRDA patterns are not associated with deeply comatose states. IRDA tends to occur in the frontal regions in adults (frontal intermittent rhythmic delta activity, or FIRDA) and in the occipital regions in (occipital intermittent rhythmic delta activity, or OIRDA) [10].

2.1.2 Prolonged bursts of slow-wave activity

Prolonged bursts of slow-wave activity can occur in a variety of etiologies in coma. They are most often diffuse but can also be lateralized without any spatiotemporal evolution [11].

2.1.3 Stimulus-induced rhythmic, periodic, or ictal discharges (SIRPIDs)

Stimulus-induced rhythmic, periodic, or ictal discharges (SIRPIDs) are a relatively common phenomenon found on prolonged electroencephalogram (EEG) monitoring that captures state changes and stimulation of comatose patients. Common causes include hypoxic injury, traumatic brain injury, and hemorrhage and toxic-metabolic disturbances [12, 13].

2.1.4 Generalized periodic and rhythmic discharges

Generalized periodic discharges (Figure 1) (GPDs) with a triphasic morphology have been associated with nonepileptic encephalopathies.

Figure 1.

A 45-year female patient coma due to intoxication with olanzapine continuous very regularly generalized 2–3/s spike and sharp wave activities.

2.1.5 Lateralized periodic discharges

PLEDs (Figure 2) are usually associated with obtundation in 95% of patients, focal seizures and focal neurological signs may occur in 80%, and Epilepsia partialis continua in 30% of the patients [14, 15].

Figure 2.

A 40-year female, mentally retarded and epileptic patient admitted to our clinic with psychosis and diagnosed as limbic encephalitis. Lateralized periodic discharges left hemisphere. Flat periods with 1- to 2-second duration.

2.1.6 Triphasic waves (TWs)

Triphasic waves (Figure 3) are periodic and generalized, typically frontally predominant and not always epileptiform in appearance. This pattern can occur in any toxic-metabolic or structural encephalopathy although the early descriptions associated its presence to hepatic encephalopathy [16, 17].

Figure 3.

A 61-year female patient, comatose state, had left-sided craniotomy after glioblastoma; EEG prominent in the left frontocentral region sharp waves with triphasic appearance.

2.1.7 Burst suppression patterns

Burst-suppression (Figure 4) in the electroencephalogram (EEG) is characterized by high amplitude events (bursts) alternated by periods of low or absent activity (suppressions). This pattern can be physiological, for instance during early development, or pathological, for example in almost half of comatose patients within the first 48 h after cardiac arrest Burst suppression pattern can also be found in various etiologies (structural, toxic, and metabolic) or during hypothermia [18].

Figure 4.

A 70-year male patient, coma after cardiac arrest; EEG shows burst suppression pattern with bursts of mixed frequencies and interposed spikes and sharp waves. No response to treatment and died 7 days later.

2.1.8 Alpha and theta coma patterns

Alpha coma can also be seen in intoxication (barbiturates, benzodiazepines, anesthetic agents, imipramine), brainstem lesions, locked-in syndrome and hypoxic-ischemic encephalopathy. Theta coma refers to the diffuse background activity of 4–7 Hz in coma. Theta coma patterns in patients with cortical dysfunction, such as in dementia or mild to moderate encephalopathy [19, 20].

2.1.9 Spindle coma patterns

Spindle coma patterns (Figure 5) in spindles, slow activity and K-complexes. They have been initially described in brain trauma but can be found also with other etiologies The etiology of spindle coma may be traumatic brain injury, intracerebral hemorrhage, post-ictal stages and intoxication [21, 22].

Figure 5.

A 45-year male patient, coma after traumatic brain injury; EEG shows 2-3 Hz delta slow waves with spindle prominent in the left frontocentral region.

3. EEG criteria for NCSE in the comatose patients

Various EEG criteria have been used in previous studies to identify patients in comatose-NCSE, yielding a prevalence between 5 and 48%, but the true incidence of NCSE in coma is still not known. Nonconvulsive status epilepticus (NCSE) is a neurological emergency that is seen in a wide spectrum of cases. Diagnosis cannot be made without electroencephalography (EEG) due to the diversity of the clinical picture and the impaired consciousness due to the underlying primary damage, especially in intensive care patients. 4. In the London-Innsbruck Status Epilepticus meeting, the previous terminology was reviewed and Salzburg Criteria for the diagnosis of NCSE by Leitinger et al. reported [23, 24, 25, 26] (Table 2).

Table 2.

The Salzburz consensus criteria for nonconvulsive stress epilepticus (NCSE).

* Typical spatiotemporal evolution.

In comatose patients, epileptiform discharges faster than 2.5 Hz or generalized periodic discharges (GPDs), lateralized periodic discharges (LPDs) and continuous 2/s GPDs with triphasic morphology of less than 2.5 Hz, as well as rhythmic discharges (RDs) faster than 0.5 Hz were also taken into consideration as NCSE if they responded to benzodiazepine treatment with improvement in the EEG or mental status of patient (Figure 6) [26, 27].

Figure 6.

(a) A 62-year female patient with breast cancer; confused; no abnormal movements; EEG shows repetitive generalized, >2.5/s spikes and slow waves with triphasic appearance. (b) Improvement of level of consciousness and EEG features following diazepam 10 mg IV.

NCSE with coma can be accompanied by generalized epileptiform discharges (coma-GED) and coma with lateralized epileptiform discharges (coma-LED). Etiologic factors and EEG patterns found in coma-GED and coma-LED are given in [19, 28] (Table 3).

Table 3.

Etiologic factors and EEG pattern in comatose NCSE.

4. Conclusion

NCSE is a disorder comprising a broad clinical spectrum that requires characteristic electroencephalographic changes to confirm the correct diagnosis. NCSE is an under-recognized cause of coma and traditionally involves the clinical picture of an altered mental status with diminished responsiveness, a diagnostic EEG and often a response to antiepileptic therapy [29].

Mortality in nonconvulsive status epilepticus can be seen in 18–25%, and in severe patients with systemic disease followed by intensive care, this rate can increase to 50–52% [24]. It is important to decide how aggressive the treatment of NCSE in a coma should be. A distinction should be made between patients in coma and other severe illnesses and those in which epileptic mechanisms actually play a role, and treatment should be guided accordingly [30].

Prognosis is better in patients with a history of epilepsy and prognosis in acutely symptomatic patients is related to the underlying disease. Convulsive and NCSE in patients with stroke, subarachnoid hemorrhage and traumatic brain injury worsen the prognosis by acting synergistically with acute brain pathology [31, 32].

NCSE is a neurological emergency that can be treated if diagnosed properly. Diagnostic criteria depend on clinical status, EEG findings and response to treatment. EEG imaging is crucial for patients with acute confusion during the initial evaluation [33].

Acknowledgments

We would like to thank Neutec company for its support in publishing this section.

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Demet Ilhan Algın, Gülgun Uncu, Demet Ozbabalık Adapınar and Oğuz Osman Erdinç (November 5th 2019). Nonconvulsive Status Epilepticus and Coma [Online First], IntechOpen, DOI: 10.5772/intechopen.89428. Available from:

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