Prevalence and factors associated with convulsive status epilepticus in Africans with epilepsy
Symon M. KariukiAngelina Kakooza‐MwesigeRyan G. WagnerEddie ChengoSteven M. WhiteGathoni KamuyuAnthony NgugiJosemir W. SanderBrian G.R. NevilleCharles R. NewtonRyan G. WagnerRhian TwineMyles ConnorFrédéric OliveMark CollinsonKathleen KahnStephen TollmanHonratio MasanjaAlexander MathewAngelina KakoozaGeorge PariyoStefan PetersonDonald NdyomughenyiSymon M. KariukiAnthony NgugiRachael OdhiamboEddie ChengoMartin ChabiEvasius BauniGathoni KamuyuVictor Mung’ala OderaJames O MagetoCharles R. NewtonKen Ae-NgibiseBright AkpaluAlbert AkpaluFrancis AgbokeyPatrick AdjeiSeth Owusu‐AgyeiChristian BottomleyImmo KleinschmidtVictor DokuPeter OdermattBrian NevilleJosemir W. SanderSteve WhiteThomas B. NutmanPatricia P. WilkinsJohn Noh
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Abstract:
We conducted a community survey to estimate the prevalence and describe the features, risk factors, and consequences of convulsive status epilepticus (CSE) among people with active convulsive epilepsy (ACE) identified in a multisite survey in Africa.We obtained clinical histories of CSE and neurologic examination data among 1,196 people with ACE identified from a population of 379,166 people in 3 sites: Agincourt, South Africa; Iganga-Mayuge, Uganda; and Kilifi, Kenya. We performed serologic assessment for the presence of antibodies to parasitic infections and HIV and determined adherence to antiepileptic drugs. Consequences of CSE were assessed using a questionnaire. Logistic regression was used to identify risk factors.The adjusted prevalence of CSE in ACE among the general population across the 3 sites was 2.3 per 1,000, and differed with site (p < 0.0001). Over half (55%) of CSE occurred in febrile illnesses and focal seizures were present in 61%. Risk factors for CSE in ACE were neurologic impairments, acute encephalopathy, previous hospitalization, and presence of antibody titers to falciparum malaria and HIV; these differed across sites. Burns (15%), lack of education (49%), being single (77%), and unemployment (78%) were common in CSE; these differed across the 3 sites. Nine percent with and 10% without CSE died.CSE is common in people with ACE in Africa; most occurs with febrile illnesses, is untreated, and has focal features suggesting preventable risk factors. Effective prevention and the management of infections and neurologic impairments may reduce the burden of CSE in ACE.Keywords:
Cross-sectional study
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Status epilepticus has been defined as `seizures so severe as to constitute a fixed and lasting condition. Prevention of status epilepticus is one of the reasons given for administering anticonvulsant drugs to children. Because status epilepticus is widely believed to be capable of producing neurologic deficit, seizures are believed to require emergency treatment to prevent status epilepticus that might cause brain damage. However, when was the last time you saw a child with status epilepticus who died or had residual encephalopathy? Certainly, there was the child who nearly drowned; the drowning caused both damage to the brain and status epilepticus. I would attribute the residual brain damage to the drowning, not to the status epilepticus.
Brain damage
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Status epilepticus has been defined as `seizures so severe as to constitute a fixed and lasting condition." Prevention of status epilepticus is one of the reasons given for administering anticonvulsant drugs to children. Because status epilepticus is widely believed to be capable of producing neurologic deficit, seizures are believed to require emergency treatment to prevent status epilepticus that might cause brain damage. However, when was the last time you saw a child with status epilepticus who died or had residual encephalopathy? Certainly, there was the child who nearly drowned; the drowning caused both damage to the brain and status epilepticus. I would attribute the residual brain damage to the drowning, not to the status epilepticus.
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A patient in status epilepticus has continuous or rapidly repeating seizures. Although the danger of this pattern of seizure activity has been recognized since antiquity, our understanding of the pathophysiology of status epilepticus is incomplete. The frequency of cases in the United States is approximately 102,000 to 152,000 per year, and roughly 55,000 deaths are associated with status epilepticus annually.1 Twelve to 30 percent of adult patients with a new diagnosis of epilepsy first present in status epilepticus.2,3 This review focuses on generalized status epilepticus, which is the most common form of the disorder.1,4 This is a life-threatening . . .
Pathophysiology
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Status epilepticus is a common neurological emergency. We report a fifty year old male who presented in status epilepticus with twenty five episodes per day which lasted for four days. This was controlled by using two hundred mg of zolpidem per day, which was subsequently slowly weaned off.
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Epilepsy syndromes
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Nonconvulsive status epilepticus includes three clinical situations: complex partial status epilepticus; absence status epilepticus; and obtundation in the presence of electrographic status epilepticus. Animal models that provide information helpful to clinical management exist for both complex partial and absence status epilepticus. In models of complex partial status epilepticus (pilocarpine, kainic acid, and various protocols using electrical stimulation), neuronal damage in discrete neuronal populations follows an episode of status epilepticus. Hippocampal populations are particularly susceptible to neuropathologic sequelae. Although it is difficult in some cases to distinguish whether the inducing agent or the status epilepticus causes neuropathology, the similar patterns of damage caused by different inducing stimuli provide converging lines of evidence suggesting that the neuropathologic consequences stem at least in part from status epilepticus. In models of absence status epilepticus (genetic mutants, pentylenetetrazole), there is relatively scarce neuropathology that can be attributed directly to status epilepticus. Together these data from animal models suggest that neuropathologic consequences from complex partial status epilepticus may be more severe than those from absence status epilepticus. If these findings translate to patients, then nonconvulsive status epilepticus of the complex partial type should be managed more aggressively than nonconvulsive status epilepticus of the absence type.
Neuropathology
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