Initial treatment of nonconvulsive status epilepticus neupsy key anoxia cerebral

There is abundant evidence from clinical studies and animal models as to the deleterious effect of on-going seizure activity in the context of CSE [ 3, 5, 18, 19], necessitating prompt intervention and treatment [ 1]. In contrast, there is much debate concerning the evidence for neuronal damage in NCSE [ 15, 16]. Moreover, the decision to treat is based on the risk–benefit ratio, whereby the efficacy of an intervention has been firmly established and the benefits outweigh any potential risks or the risk of nonintervention [ 9]. Ultimately, the decision whether treatment is initiated or not is predicated on whether a reliably effective treatment exists and whether failure to treat results in on-going deleterious cerebral effects and consequently increased morbidity and mortality.Anoxia cerebral


we will examine the evidence for efficacy and necessity of treatment for the four main individual subtypes of NCSE, namely typical absence status epilepticus, simple partial status epilepticus, CPSE, and NCSE in coma. Lastly, we will address the issue of use of anesthesia in NCSE.

Typical absence status epilepticus (ASE) usually occurs in children or adolescents with an idiopathic generalized epilepsy (IGE) or those with a history of an IGE in childhood; it can, however, sometimes occur de novo or as a late presentation of IGE in the elderly [ 20]. It manifests as varying degrees of alteration in mental status or behavior. This is associated with the classical EEG pattern of large symmetrical bilateral synchronous 2.5–3 hz spike and wave discharges, although this pattern may become discontinuous the longer it persists.Anoxia cerebral the natural history of typical ASE is a duration of several hours, with spontaneous cessation, although it can persist several days, ending in a generalized convulsive seizure in up to a third of cases. Typical absence status is often precipitated by anti-seizure drug (ASD) withdrawal, or ASD non-adherence—with re-instatement of therapy a significant component of management. Typical ASE can also be precipitated by the use of inappropriate asds such as carbamazepine or phenytoin [ 21].

Acute treatment of ASE is, therefore, mostly aimed at preventing injury due to the altered conscious state or the occurrence of a convulsion. The consensus is that ASE responds rapidly to treatment with oral or IV benzodiazepines [ 6, 7, 9, 27] particularly clonazepam [ 27] (table 22.2 [ 10, 31]), or IV valproate or oral acetazolamide when benzodiazepines are contraindicated.Anoxia cerebral moreover, successful management requires identification and correction of and avoidance of potential precipitating factors, if possible, such as acute systemic infections, psychotropic drugs, use of inappropriate asds, or alcohol withdrawal [ 26, 27, 29, 32]. Interestingly, episodes of ASE may be triggered by use of inappropriate asds such as carbamazepine and phenytoin which may render standard treatment [benzodiazepines (bzds) or valproic acid (VPA)] ineffective due to a paradoxical effect of the inappropriate ASD, underscoring the risk of iatrogenic exacerbation of ASE [ 21, 33]. For people with IGE prone to recurrent episodes of typical ASE, long-term therapy appears to be efficacious in significantly reducing or preventing further attacks [ 34].Anoxia cerebral the elderly with NCSE de novo rarely require longer term treatment.

Simple partial status epilepticus (SPSE) or aura continua is considered a rare form of SE, but because it lacks motor features or impairment of consciousness, it may go unrecognized. SPSE arises as a result of seizure activity involving a focal area of cortex, with diverse clinical presentations including aphasia, visual or auditory hallucinations, altered perception, transient visual loss, and episodes of fear. Similarly, SPSE may take the form of focal motor seizures, aversive eye movements, transient paralysis contralateral to the epileptic focus, or focal myoclonic jerks with or without impairment of consciousness ( epilepsia partialis continua [EPC]) lasting days to months—which may be highly refractory to treatment [ 36].Anoxia cerebral in the largest reported series, among 47 people with new onset SPSE identified retrospectively over a 5-year period in the netherlands, all but one (with aphasia) had somatomotor SPSE; 20 had EPC. Just over half (27) had a previous diagnosis of epilepsy, although the SPSE was caused by a new neurologic diagnosis in six. Of those without a prior diagnosis of epilepsy, cerebrovascular disease was the most common etiology of SPSE, in 14 patients. Overall, four patients died (all due to acute cerebrovascular disease) and ten had associated morbidity, only one case of which was felt to be attributable to the SPSE. In general, SPSE appears to be associated with low mortality and morbidity, almost always caused primarily by the underlying etiology.Anoxia cerebral treatment, first with oral or IV bzds (e.G. Clonazepam) followed, if necessary, by IV phenytoin, is usually effective (table 2). Anesthesia should, if possible, be avoided in patients with SPSE (see below).

Complex partial status epilepticus (CPSE) is in contrast probably the most frequent subtype of NCSE, reportedly accounting for up to 40% of cases of SE overall [ 12, 37]. The presentation of CPSE can be very heterogeneous and primarily determined by the origin of the epileptic focus. Fluctuating consciousness, with or without amnesia is the typical presentation, but altered consciousness may not occur in CPSE with a unilateral frontal lobe focus [ 38]. It can be difficult to distinguish CPSE from ASE, especially in the elderly with de novo ASE.Anoxia cerebral moreover, while CPSE needs to be differentiated from other forms of NCSE, it also needs to be distinguished from other causes of encephalopathy (e.G., hepatic encephalopathy), prolonged post-ictal states, or primarily psychiatric behavioral changes. This is often not straightforward. EEG is not always helpful, as the changes on scalp EEG in CPSE can be relatively nonspecific, so the diagnosis of CPSE remains primarily an electro-clinical one. Nevertheless, strict electrographic criteria for the diagnosis of CPSE need to be employed [ 39, 40].

This and other case series of CPSE [ 38, 42– 44] suggest a relatively favorable prognosis in terms of neurocognitive sequelae. CPSE in those with prior epilepsy is typically responsive to oral bzds such as clobazam or intravenous bzds such as lorazepam or diazepam, although recurrence is not uncommon [ 42].Anoxia cerebral there may, however, be a delayed clinical response despite resolution of EEG features as the patient enters a post-ictal state. Consequently, EEG monitoring, when available, should be used to monitor the response to treatment. In the case of failure of response to oral or IV bzds, IV asds can be considered [ 48, 49] (see table 22.2). In the scenario where CPSE with prior epilepsy remains refractory to non-anesthetic agents, treatment escalation to IV anesthetics should only be considered with caution and on an individual basis. The paucity of clinical data for long-term neurocognitive consequences underlies the reticence of many neurologists to advocate escalation to IV anesthetic agents, given their association with morbidity and mortality [ 50].Anoxia cerebral

De novo CPSE, occurring in the context of acute or progressive neurological conditions, is in contrast, often refractory to non-anesthetic agents. Prognosis, as with generalized CSE [ 51], is primarily determined by the underlying etiology, and successful management of the CPSE is contingent on the rapid recognition of the precipitating cause if possible. This is particularly true in the case of autoimmune encephalitis, such as anti-NMDA receptor encephalitis, which can result in CPSE resistant to standard asds and IV anesthetic agents, responding only after initiation of immunosuppressive therapy (IV steroids, IVIG, or plasma exchange) [ 52]. Because of the potential response of these conditions to immunosuppression, autoimmune encephalitis should be considered in all patients with SE and encephalitis of unknown origin, with early use of immunosuppression when there is a high clinical suspicion.Anoxia cerebral in all these cases, suitable examination and investigation should be performed to look for occult tumors (in particular ovarian, breast, and testes).

Despite the significant morbidity and mortality associated with NCSE in coma there are few data to guide management or indeed, to inform us if intervention even impacts overall prognosis. “subtle” NCSE is considered the most malignant form of NCSE, the management of which was studied in the veteran’s affairs status epilepticus study [ 54], where 570 patients with SE (375 with overt SE, and 175 with subtle SE) were randomized to one of four treatment arms: administration of lorazepam (0.1 mg/kg); diazepam (0.15 mg/kg) followed by phenytoin (18 mg/kg); phenobarbital (18 mg/kg); or phenytoin (18 mg/kg) alone.Anoxia cerebral successful cessation of SE was significantly better for overt SE compared to subtle SE in all four treatment arms: lorazepam (67% for overt SE, compared to 26.1% for subtle SE); phenobarbital (63% compared to 24.4%); diazepam and phenytoin (59.6% compared to 23.4%) and phenytoin (51% compared to 19.5%). While lorazepam was found superior to phenytoin in the treatment of overt SE ( p = 0.002), no difference was found between any two treatment arms for the management of subtle SE ( p = 0.18) [ 54].