Epileptic seizures resulting from acute cerebral anoxia

Madison, David S.; Niedermeyer, E.

doi:10.1136/jnnp.33.3.381

Cited by 70 publications

(26 citation statements)

References 13 publications

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“…The semiology of seizures in comatose patients is rarely generalized tonic-clonic; rather, it is more often focal clonic, or myoclonic, inconspicuous, and limited to only some parts of the body, face, or eyes [134]. Myoclonic jerks are most often encountered in deep coma, specifically after hypoxic/anoxic brain injury [135][136][137][138][139][140]. The EEG sometimes does not reveal accompanying ictal activity; hence, the question whether these clinical activities were epileptic phenomena or not remains unresolved.…”

Section: Ictal Semiology In Comamentioning

confidence: 97%

Which EEG patterns in coma are nonconvulsive status epilepticus?

Trinka¹,

Leitinger²

2015

Epilepsy & Behavior

139

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Nonconvulsive status epilepticus (NCSE) is common in patients with coma with a prevalence between 5% and 48%. Patients in deep coma may exhibit epileptiform EEG patterns, such as generalized periodic spikes, and there is an ongoing debate about the relationship of these patterns and NCSE. The purposes of this review are (i) to discuss the various EEG patterns found in coma, its fluctuations, and transitions and (ii) to propose modified criteria for NCSE in coma. Classical coma patterns such as diffuse polymorphic delta activity, spindle coma, alpha/theta coma, low output voltage, or burst suppression do not reflect NCSE. Any ictal patterns with a typical spatiotemporal evolution or epileptiform discharges faster than 2.5 Hz in a comatose patient reflect nonconvulsive seizures or NCSE and should be treated. Generalized periodic diacharges or lateralized periodic discharges (GPDs/LPDs) with a frequency of less than 2.5 Hz or rhythmic discharges (RDs) faster than 0.5 Hz are the borderland of NCSE in coma. In these cases, at least one of the additional criteria is needed to diagnose NCSE (a) subtle clinical ictal phenomena, (b) typical spatiotemporal evolution, or (c) response to antiepileptic drug treatment. There is currently no consensus about how long these patterns must be present to qualify for NCSE, and the distinction from nonconvulsive seizures in patients with critical illness or in comatose patients seems arbitrary. The Salzburg Consensus Criteria for NCSE [1] have been modified according to the Standardized Terminology of the American Clinical Neurophysiology Society [2] and validated in three different cohorts, with a sensitivity of 97.2%, a specificity of 95.9%, and a diagnostic accuracy of 96.3% in patients with clinical signs of NCSE. Their diagnostic utility in different cohorts with patients in deep coma has to be studied in the future. This article is part of a Special Issue entitled "Status Epilepticus".

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Section: Ictal Semiology In Comamentioning

confidence: 97%

Which EEG patterns in coma are nonconvulsive status epilepticus?

Trinka¹,

Leitinger²

2015

Epilepsy & Behavior

139

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“…For example, Schiff & Somjen (1985) found that hippocampal cells were hyperexcitable for up to 45 min after a brief exposure to hypoxia. There have also been reports of neuronal hyperexcitability following post-hypoxic epilepsy (Madison & Niedermeyer, 1970) and monoclonus (Lance & Adams, 1963). An important aspect of these studies was that the hyperexcitability persisted for a relatively long time following the hypoxic insult.…”

Section: Discussionmentioning

confidence: 99%

Two long‐lasting central respiratory responses following acute hypoxia in glomectomized cats.

Gallman¹,

Millhorn²

1988

The Journal of Physiology

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SUMMARY1. Central respiratory response to acute (10 min) hypoxia, as measured by phrenic nerve activity, was determined in peripheral chemo-denervated cats.2. Hypoxia was induced by ventilating cats for 10 min at reduced inspired oxygen levels (inspired 02 fraction, FI°2 = 0-06-0-15). The degree of hypoxaemia was determined from an arterial blood sample and ranged from 'severe' (arterial 02 pressure, Pa,°< 26 Torr) to 'mild' (Pa, 02 > 35 Torr). The respiratory response was monitored for 1 h following return to ventilation with 100 % oxygen.3. The results confirmed the finding of prolonged ( > 60 min) inhibition of respiration upon return to hyperoxic conditions following severe hypoxia, as reported previously (Millhorn, Eldridge, Kiley & Waldrop, 1984). A new finding was a long-lasting ( > 60 min) facilitation of respiration following exposure to less severe (Pa, 02 > 35 Torr) hypoxia.4. Medullary extracellular fluid pH was measured in six cats. Changes in pH could not explain either the prolonged inhibition following severe hypoxia or the longlasting facilitation observed following mild hypoxia.5. Ablation studies were performed in order to determine the locations of the neuronal substrates for the inhibitory and facilitatory mechanisms. The results of this series of experiments indicate that the mesencephalon is necessary for activation of the inhibitory mechanism, while the facilitatory mechanism requires the presence of higher brain structures, notably the diencephalon.6. Following removal of the diencephalon, the inhibitory response was seen following even mild hypoxic insults, i.e. those shown to produce facilitation in animals with intact brains. In the absence of the mesencephalon, neither prolonged inhibition nor prolonged facilitation could be produced following hypoxia.7. It is proposed that there are two centrally mediated long-lasting responses to acute hypoxia. Facilitation is seen following mild hypoxia. Inhibition is more likely following severe hypoxia. However, both mechanisms appear to be triggered simultaneously and the output of the central respiratory controller reflects the influence of each.

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“…This was an unprecedented case of documented spikes with a central focus in acute postanoxic myoclonus. There have been cases of vertex, central, and frontal-dominant generalized spikes, 10 and there might be a lack of reports Seongheon Kim, et al Recurred myoclonic SE in hypoxic encephalopathy after SSEP due to difficulty ascertaining these discharges in the midst of myoclonic artifacts. Acute postanoxic myoclonus may either occur spontaneously or with sensory stimuli, somatosensory stimuli being the most common.…”

Section: Discussionmentioning

confidence: 99%

Myoclonic status epilepticus in hypoxic ischemic encephalopathy which recurred after somatosensory evoked potential testing

Kim

et al. 2017

Ann Clin Neurophysiol

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Epileptic seizures resulting from acute cerebral anoxia

Cited by 70 publications

References 13 publications

Which EEG patterns in coma are nonconvulsive status epilepticus?

Which EEG patterns in coma are nonconvulsive status epilepticus?

Two long‐lasting central respiratory responses following acute hypoxia in glomectomized cats.

Myoclonic status epilepticus in hypoxic ischemic encephalopathy which recurred after somatosensory evoked potential testing

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