scholarly journals Concepts in Periodic Discharges: A Descriptive Study

2018 ◽  
Vol 05 (02) ◽  
pp. 068-074
Author(s):  
Laxmi Khanna ◽  
Nandini Agarwal ◽  
Sabita Kandel

Abstract Introduction Periodic discharges are now known as the ictal–interictal continuum and represent ongoing injury in acute or chronic neurological illnesses. Objective The aim of our study was to identify periodic discharges in patients who have undergone continuous bedside electroencephalography (EEG) monitoring and to classify the EEG according to the current American Clinical Neurophysiology Society terminology. Materials and Methods The continuous bedside EEG records of intensive care patients admitted from August 2017 to July 2018 were analyzed. The clinical spectrum, the treatment, and outcome of each of these patients were monitored. Results Fifty cases of periodic discharges (11 children, 39 adults) were identified over 1 year from 2017 to 2018. The clinical presentation included 32% seizures, 16% status epilepticus, 20% coma, 16% fever with altered sensorium, 8% abnormal behavior, 4% strokes, and 4% traumatic brain injury. The diagnosis was 20% autoimmune encephalitis, 8% herpes encephalitis, 20% multiorgan failure, 4% traumatic brain injury, 16% status epilepticus, 16% posthypoxic encephalopathy, 4% strokes, 4% intracerebral bleeds, 4% meningitis, and 4% severe dementia. Lateralized periodic discharges were identified in 20%, bilateral independent periodic discharges in 20%, and generalized periodic discharges in 60%. Fifty-six percent patients recovered with residual neurological deficits and 44% succumbed to their illness. Conclusions Continuous bedside EEG monitoring has revolutionized the approach to seizures in critically ill patients. Despite a vigilant approach and diligent diagnosis of these abnormal rhythms, the mortality rate was 20% in patients with lateralized periodic discharges and 60% with bilateral and generalized periodic discharges (p ≤ 0.05).

1999 ◽  
Vol 91 (5) ◽  
pp. 750-760 ◽  
Author(s):  
Paul M. Vespa ◽  
Marc R. Nuwer ◽  
Valeriy Nenov ◽  
Elisabeth Ronne-Engstrom ◽  
David A. Hovda ◽  
...  

Object. The early pathophysiological features of traumatic brain injury observed in the intensive care unit (ICU) have been described in terms of altered cerebral blood flow, altered brain metabolism, and neurochemical excitotoxicity. Seizures occur in animal models of brain injury and in human brain injury. Previous studies of posttraumatic seizures in humans have been based principally on clinical observations without a systematic approach to electroencephalographic (EEG) recording of seizures. The purpose of this study was to determine prospectively the incidence of convulsive and nonconvulsive seizures by using continuous EEG monitoring in patients in the ICU during the initial 14 days postinjury.Methods. Ninety-four patients with moderate-to-severe brain injuries underwent continuous EEG monitoring beginning at admission to the ICU (mean delay 9.6 ± 5.4 hours) and extending up to 14 days postinjury. Convulsive and nonconvulsive seizures occurred in 21 (22%) of the 94 patients, with six of them displaying status epilepticus. In more than half of the patients (52%) the seizures were nonconvulsive and were diagnosed on the basis of EEG studies alone. All six patients with status epilepticus died, compared with a mortality rate of 24% (18 of 73) in the nonseizure group (p < 0.001). The patients with status epilepticus had a shorter mean length of stay (9.14 ± 5.9 days compared with 14 ± 9 days [t-test, p < 0.03]). Seizures occurred despite initiation of prophylactic phenytoin on admission to the emergency room, with maintenance at mean levels of 16.6 ± 2.8 mg/dl. No differences in key prognostic factors (such as the Glasgow Coma Scale score, early hypoxemia, early hypotension, or 1-month Glasgow Outcome Scale score) were found between the patients with seizures and those without.Conclusions. Seizures occur in more than one in five patients during the 1st week after moderate-to-severe brain injury and may play a role in the pathobiological conditions associated with brain injury.


1999 ◽  
Vol 7 (3) ◽  
pp. E1 ◽  
Author(s):  
Paul M. Vespa ◽  
Marc R. Nuwer ◽  
Valeriy Nenov ◽  
Elisabeth Ronne-Engstrom ◽  
David A. Hovda ◽  
...  

Object The early pathophysiological features of traumatic brain injury observed in the intensive care unit (ICU) have been described in terms of altered cerebral blood flow, altered brain metabolism, and neurochemical excitotoxicity. Seizures occur in animal models of brain injury and in human brain injury. Previous studies of posttraumatic seizures in humans have been based principally on clinical observations without a systematic approach to electroencephalographic (EEG) recording of seizures. The purpose of this study was to determine prospectively the incidence of convulsive and nonconvulsive seizures by using continuous EEG monitoring in patients in the ICU during the initial 14 days postinjury. Methods Ninety-four patients with moderate-to-severe brain injuries underwent continuous EEG monitoring beginning at admission to the ICU (mean delay 9.6 ± 5.4 hours) and extending up to 14 days postinjury. Convulsive and nonconvulsive seizures occurred in 21 (22%) of the 94 patients, with six of them displaying status epilepticus. In more than half of the patients (52%) the seizures were nonconvulsive and were diagnosed on the basis of EEG studies alone. All six patients with status epilepticus died, compared with a mortality rate of 18 (24%) of 73 in the nonseizure group (p < 0.001). The patients with status epilepticus had a shorter mean length of stay (9.14 ± 5.9 days compared with 14 ± 9 days (t-test, p < 0.03). Seizures occurred despite initiation of prophylactic phenytoin on admission to the emergency room, with maintenance at mean levels of 16.6 ± 2.8 mg/dl. No differences in key prognostic factors (such as the Glasgow Coma Scale score, early hypoxemia, early hypotension, or 1-month Glasgow Outcome Scale score) were found between the patients with seizures and those without. Conclusions Seizures occur in more than one in five patients during the 1st week after moderate-to-severe brain injury and may play a role in the pathobiological conditions associated with brain injury.


2020 ◽  
Vol 11 ◽  
Author(s):  
Fangfang Bi ◽  
Huaifen Ma ◽  
Chen Ji ◽  
Cuicui Chang ◽  
Wenbo Liu ◽  
...  

2021 ◽  
Vol 121 (5) ◽  
pp. 62
Author(s):  
M.V. Sinkin ◽  
A.E. Talypov ◽  
A.A. Yakovlev ◽  
O.O. Kordonskaya ◽  
A.M. Teplyshova ◽  
...  

2019 ◽  
Vol 36 (11) ◽  
pp. 1890-1907 ◽  
Author(s):  
Pedro Andrade ◽  
Ivette Banuelos-Cabrera ◽  
Niina Lapinlampi ◽  
Tomi Paananen ◽  
Robert Ciszek ◽  
...  

2019 ◽  
Vol 20 (24) ◽  
pp. 6125 ◽  
Author(s):  
Ning Liu ◽  
Yinghua Jiang ◽  
Joon Yong Chung ◽  
Yadan Li ◽  
Zhanyang Yu ◽  
...  

Our laboratory and others previously showed that Annexin A2 knockout (A2KO) mice had impaired blood–brain barrier (BBB) development and elevated pro-inflammatory response in macrophages, implying that Annexin A2 (AnxA2) might be one of the key endogenous factors for maintaining homeostasis of the neurovascular unit in the brain. Traumatic brain injury (TBI) is an important cause of disability and mortality worldwide, and neurovascular inflammation plays an important role in the TBI pathophysiology. In the present study, we aimed to test the hypothesis that A2KO promotes pro-inflammatory response in the brain and worsens neurobehavioral outcomes after TBI. TBI was conducted by a controlled cortical impact (CCI) device in mice. Our experimental results showed AnxA2 expression was significantly up-regulated in response to TBI at day three post-TBI. We also found more production of pro-inflammatory cytokines in the A2KO mouse brain, while there was a significant increase of inflammatory adhesion molecules mRNA expression in isolated cerebral micro-vessels of A2KO mice compared with wild-type (WT) mice. Consistently, the A2KO mice brains had a significant increase in leukocyte brain infiltration at two days after TBI. Importantly, A2KO mice had significantly worse sensorimotor and cognitive function deficits up to 28 days after TBI and significantly larger brain tissue loss. Therefore, these results suggested that AnxA2 deficiency results in exacerbated early neurovascular pro-inflammation, which leads to a worse long-term neurologic outcome after TBI.


Author(s):  
Martin Beed ◽  
Richard Sherman ◽  
Ravi Mahajan

Decreased consciousnessSeizures and status epilepticusStroke/thromboembolic strokeIntracerebral haemorrhageSubarachnoid haemorrhageTraumatic brain injuryRaised intracranial pressureMeningitis and encephalitisAgitation/confusion/aggressionAlcohol withdrawalNeuromuscular weakness and paralysisGuillain–Barré syndromeMyasthenia gravis↓consciousness occurs in many diseases requiring admission to intensive care, and is often a cause for admission in its own right. Changes in neurological state may be related to intracranial pathology, or may occur in response to respiratory, circulatory, or metabolic disorders....


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