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Status epilepticus




В начале болезни припадки встречаются реже, иногда. отделяяоь один от другого ггромйжутками в несколым) меоядев; в дальнейшем оии учащаются, отмечаясь ежемесячно, еженедельно, ежедиевно и иногда no 2—3 прітпадка в день. В других случаях припадки сразу же становятся доволыю частьтми. Частота припадков нередко увеличйвастся осетіыо и зимото, в отделыгых случаях отмеча.ется периодичиость припадков, наступающих в одіш и те жѳ числа, часьт. Особеіптого вттимания заслуягивает уясе отмечеігігое нами учащеіше припадков, известное под названием status epilepticus. Здесь припадки кепрерывно следуют одиіі за другим, при этом ігередко повышается тешгсратура, доходятдая в отдельных случаях до 40°. R значительном проценте случаев status epilepticus кончается смертельньтм ттсходом, в тех же случаях, когда болыгой нопрлвляется, остается ттаклоттттостъ к повторетгттто ттодобітых состояітий. П р о г тт о з ттртт зштлепсии в общем ттеблагоприятігый. Такгте больттъте обычно тгедолговечітьт, отпі часто допібатот, как. зто уже упоминалось, от status epilepticus, от несчастиых случаер во время судорожттьтх прттпадков и сумеречгіьтх состояний созттатгия. НеблагопрігятнЬ предскаізание также и в смътсле почги иеизбежной деградации. наступления более иліг менее выраягеиіюго слабоѵмия. Необходігмо, однако, учесть и возміожиость сравнителыіо благоприятного течсиия нроцесса, вогда y больного ігрттадки редки и быватот липіь no тючам, слабоумие тіарастает мюдлошто и больные могут более иліг менее успепшо работать. [стр. 79 ⇒]

Cognitive disorders follow status epilepticus with simple partial seizures, complex partial seizures, or absence seizures. Recurrent or prolonged simple partial seizures do not result in alteration of consciousness or invariable abnormalities on EEG, and, if manifested by psychic auras, simple partial seizures may be difficult to distinguish from primary psychiatric disturbances. Status epilepticus from complex partial seizures and absence seizures results in prolonged alterations of responsiveness. With the addition of various ictal auras, complex partial status epilepticus can appear psychotic. Occasionally, EEGs and a therapeutic trial of anticonvulsant medications may be the only way to distinguish behavioral disturbances caused by nonconvulsive status epilepticus. Finally, recurrent EEG complexes known as periodic lateralizing epileptiform discharges may also be associated with prolonged confusional behavior and focal cognitive changes. [стр. 636 ⇒]

 Hanley D.F., Kross J.F. Use of midazolam in the treatment of refractory status epilepticus // Clin. Ther. — 1998. — Vol. 20. — P. 1093. 17. Uberall M.A., Trollmann R., Wunsiedler U., Wenzel D. Intravenous valproate in pediatric epilepsy patients with refractory status epilepticus // Neurology. — 2000. — Vol. 54. — P. 2188. [стр. 223 ⇒]

Generalized convulsive status epilepticus (GCSE) is defined as recurrent seizures without recovery of consciousness lasting more than 30 minutes or when seizure activity becomes unremitting (Fig. 14-8). One of the most common and lifethreatening neurologic emergencies, GCSE mandates immediate treatment because of the potential for irreversible CNS damage, that is, neuronal loss secondary to anoxia and systemic metabolic and autonomic dysfunction. Medical complications such as cardiac arrhythmias, pulmonary edema, and renal failure sometimes occur in association with GCSE. The GCSE mortality rate approaches 30%. Unfortunately, the history in the above vignette in this chapter is common in patients with partial seizures with secondary generalization who do not comply with antiepileptic therapy and progress to status epilepticus. Treatment of GCSE treatment requires the maintenance of an adequate airway, ventilation, and circulatory support and the termination of seizures. Etiologic mechanisms include anticonvulsant or other medication withdrawal, illicit toxic drugs, hypoglycemia, hyponatremia, and hypocalcemia. GCSE may be the first manifestation of acute cerebral pathology. The initial therapy, a benzodiazepine or phenytoin, often depends on whether the patient is actively seizing. Both firstline medications are frequently utilized within a short time. Intravenous lorazepam at 1–2 mg every 1–2 minutes up to 8 mg or diazepam 5 mg up to 20 mg is most often the initial therapy. An infusion of phenytoin (at 50 mg/minute) or fosphenytoin (at... [стр. 191 ⇒]

Phenytoin is given with normal saline and not with glucose as it precipitates out of solution in this vehicle. ECG monitoring is required to monitor the effects of phenytoin on cardiac conduction, especially if infused too rapidly. Hypotension is also a serious side effect, especially in patients showing evidence of hemodynamic instability. The propylene glycol and alcohol content of the intravenous preparation is thought to be partially responsible for these effects and is dependent on the infusion rate. Fosphenytoin, a water-soluble phosphate ester rapidly converted to phenytoin, can be administered at a more rapid rate (150 mg/ minute of phenytoin equivalent) while minimizing the risk of cardiovascular instability in unstable patients. Fosphenytoin also has a lower incidence of pain and burning at the infusion site but its routine use remains restricted because of its high cost. If seizures persist and serum phenytoin levels drawn 20 minutes after the initial infusion are less than 20 mg/dL then additional phenytoin or fosphenytoin (5–10 mg/kg) to control seizure and maintain the level around 20–30 mg/dL may be given. Sodium valproate IV, at a loading dose of 10–15 mg/kg, has also been used successfully to control status epilepticus, especially in patients on regular regimens of oral valproic acid. Barbiturates have been traditionally used as second-line agents in status epilepticus. Long-acting phenobarbital... [стр. 192 ⇒]

Intubation for airway protection and continuous EEG monitoring are usually required at this stage. Over the years, however, many centers have shifted to using continuous infusions of other agents, such as the shortacting benzodiazepine midazolam or the hypnotic propofol (decreases excitatory effect of glutamate) for control of recurrent seizures. Many centers now use continuous infusion of benzodiazepines such as midazolam or propofol before barbiturate anesthesia is initiated. Nonconvulsive status epilepticus or absence status epilepticus is another form of continued seizures without motor accompaniments. Typically, patients are poorly responsive with decreased alertness or obtundation. EEG reveals mostly continuous generalized spike-and-wave activity, the so-called spike– wave stupor. Intravenous benzodiazepine administration, the treatment of choice, is generally effective. Complex partial seizures may occasionally evolve into complex partial status epilepticus, in which patients do not regain full consciousness between seizures. Prompt treatment as prescribed for GCSE is necessary. An SPS may evolve into epilepsia partialis continua, as described above. Long-term anticonvulsant therapy is usually needed in patients who have experienced status epilepticus. [стр. 192 ⇒]

Many genetic components are being investigated that could have potential for therapies. Clinical trials are currently underway with implantable stimulators and sensing devices that may detect, modulate, and prevent seizure discharges. ADDITIONAL RESOURCES Akanuma N, Koutroumanidis M, Adachi N, et al. Presurgical assessment of memory-related brain structures: the Wada test and functional neuroimaging. Seizure 2003;12:346-358. American Academy of Neurology; American Epilepsy Society. Practice Parameter: evaluating an apparent unprovoked first seizure in adults (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Neurology 2007 Nov 20;69(21):1996-2007. An evidence-based guide to the workup of a first-time unprovoked seizure and analysis of the predictive value of each finding. Asadi-Pooya AA, Sperling M. Antiepileptic Drugs: A Clinician’s Manual. Oxford University Press; 2009. This handbook provides practical, up-to-date information on how to select, prescribe, and monitor AEDs. Engel J Jr, Wiebe S, French J, et al. Practice parameter: temporal lobe and localized neocortical resections for epilepsy: report of the Quality Standards Subcommittee of the American Academy of Neurology, in association with the American Epilepsy Society and the American Association of Neurological Surgeons. Neurology 2003;60:538-547. Engel J Jr, Pedley TA, editors. Epilepsy: A Comprehensive Textbook. Philadelphia, Pa: Lippincott–Raven; 1998. Engel J Jr. Seizures and Epilepsy. Philadelphia, Pa: FA Davis Co; 1989. Harden CL. The adolescent female with epilepsy: mood, menstruation, and birth control. Neurology 2006;66(S3). An excellent supplement that addresses the challenges in treating women with epilepsy including the link between epilepsy and depression, risk of reproductive disorders, efficacy of hormonal contraceptives, and interactions between oral contraceptives and AEDs. Kwan P, Brodie MJ. Early identification of refractory epilepsy. N Engl J Med 2000;342(5):314-319. Meador KJ, Baker GA, Finnell RH, et al. In utero antiepileptic drug exposure: fetal death and malformations. Neurology 2006;67(3):407-412. More adverse outcomes were observed with in utero exposure to valproate compared to other AEDs suggesting that valproate poses the greatest risk to the fetus. Morrell MJ. In: Levy RH, et al, editors. Antiepileptic Drugs. 5th ed. Lippincott Wilkins & Williams; 2002. p. 132-148. An excellent reference of the mechanisms of action, chemistry, biotransformation, pharmacokinetics, interactions, use and adverse effects of AEDs. Motamedi GK, Meador KJ. Antiepileptic drugs and neurodevelopment. Cur Neurol Neurosci Rep 2006;6(4):341-346. Children with in utero exposure to valproate had a higher incidence of additional educational needs, showed a significantly lower verbal IQ, developmental delays, memory impairment, and dysmorphic features compared to other AEDs. Porter RJ, Meldrum BS. Antiseizure Drugs. In: Katzung BG, editor. Basic & Clinical Pharmacology, Lange Medical Book, McGraw-Hill. 10th ed. Chapter 24. 2006. p. 374-394. An up-to-date and complete pharmacology textbook. Rosenow F, Luders H. Presurgical evaluation of epilepsy. Brain 2001;124:1683-1700. Siegel AM. Presurgical evaluation and surgical treatment of medically refractory epilepsy. Neurosurg Rev 2004;27:1-18. Sperling MR, Feldman H, Kinman J, et al. Seizure control and mortality in epilepsy. Ann Neurol 1999;46(1):45-50. Wiebe S, Blume WT, Girvin JP, et al. A randomized controlled trial of surgery for temporal lobe epilepsy. N Engl J Med 2001;345(5):311-318. Working Group on Status Epilepticus. Treatment of convulsive status epilepticus. JAMA 1993;270:854-859. Zahn CA, Morrell MJ, Collins SD, et al. Management issues for women with epilepsy. A review of the literature. Neurology 1998;51:949-956. A review of the recommendations concerning contraception, folate supplementation, vitamin K use in pregnancy, breast feeding, bone loss, catamenial epilepsy, and reproductive endocrine disorders. [стр. 199 ⇒]

Этиология Annegers JF et al: A population-based study of seizures after traumatic brain injuries. N Engl J Med 1998;338:20-24. Berg AT et al: A prospective study of recurrent febrile seizures. N Engl J Med 1992;327:1122-1127. Burn J et al: Epileptic seizures after a first stroke: the Oxfordshire Community Stroke Project. BMJ 1997;315:1582-1587. Delanty N, Vaughan CJ, French JA: Medical causes of seizures. Lancet 1998;352:383-390. Ettinger AB, Shinnar S: New-onset seizures in an elderly hospitalized population. Neurology 1993;43: 489-492. Fox MW, Hatms RW, Davis DH: Selected neurological complications of pregnancy. Mayo Clin Proc 1990;65:1595-1618. Kurtz Z et al: Epilepsy in young people: 23 year follow up of the British national child development study. BMJ 1998;316:339-342. Leppik IE (editor): Status epilepticus in perspective. Neurology 1990;40(Suppl 2):1—51. [Entire issue.] Lowenstein DH, Alldredge BK: Status epilepticus. N Engl J Med 1998;338:970-976. Messing RO, Closson RG, Simon RP: Druginduced seizures: a 10-year experience. Neurology 1984;34:1582-1586. Messing RO, Simon RP: Seizures as a manifestation of systemic disease. Neural Clin 1986;4:563-584. Pomeroy SL et al: Seizures and other neurological sequelae of bacterial meningitis in children. N Engl J Med 1990;323:1651-1657. ferity CM et al: Long-term intellectual and behavioral outcomes of children with febrile convulsions. N Engl J Med 1998;338:1723-1728. [стр. 379 ⇒]

Status epilepticus Unless otherwise stated the term status epilepticus indicates the occurrence of one tonic–clonic seizure after another without recovery of consciousness between attacks. During tonic–clonic seizures, there exists a state of increased cerebral metabolism and oxygen requirement and decreased respiratory efficiency and cyanosis. If further tonic–clonic seizures occur at short intervals, it is easy to understand that increasing metabolic acidosis and oedema will occur in the brain, and progressively increasing coma will overtake the patient. There is evidence that, even if hypoxia and metabolic acidosis are prevented, seizures themselves can cause permanent brain damage if they last more than 1 hour (as a toxic consequence of excessive release of excitatory neurotransmitters). Hence, urgent control of seizures and attention to respiration are required in patients with tonic–clonic status, usually needing admission to an intensive care unit. The treatment is discussed in more detail on p. 208. Even with careful management, status epilepticus has a significant mortality rate and it is common for survivors to have new cognitive or physical difficulties or more refractory epilepsy. [стр. 212 ⇒]

Status epilepticus Any form of status epilepticus is an indication for hospitalization to establish control of the seizures, but in the case of tonic–clonic status the problem is a medical emergency requiring admission to an intensive care unit. There are three main directions of treatment of grand mal status: 1. Routine care of the unconscious patient (see Chapter 11, p. 187). 2. Control of seizure activity in the brain. This means the maintenance of the patient’s normal anticonvulsant regime, supplemented by the use of intravenous anticonvulsants; diazepam or lorazepam early; phenytoin or phenobarbitone if seizures persist; thiopentone to produce general anaesthesia if seizures have failed to come under control within 60 minutes. 3. Maintenance of optimal oxygenation of the blood. This may mean the use of oxygen and an airway, but may be the main indication for anaesthesia, paralysis and ventilation. It is important to remember the control of seizure activity in the brain of the paralyzed. Vigorous anticonvulsant therapy must be continued. [стр. 219 ⇒]

Case 2 a. The emergency management of status epilepticus starts with the establishment of an airway but it is generally impossible to secure this until you have controlled the seizures. You need to obtain intravenous access and administer intravenous lorazepam (or diazepam) followed by intravenous phenytoin. As the seizures subside you can insert an oral airway. b. The second phase in the management of status epilepticus is to find out the cause. The commonest is lack of concordance with medication in patients who are known to have epilepsy. When the first manifestation of epilepsy is status epilepticus, the underlying cause is often serious (tumour, stroke, etc.). The worry here is the persistent fever. It is common to have a fever during status epilepticus because of the heat generated by muscle activity. The white cell count also usually rises. But you would expect the temperature to fall subsequently, rather than to rise. He could have aspirated while fitting and have pneumonia. Ecstasy toxicity can also present in this way. But the priority is to exclude intracranial infection. His CT brain scan showed no abnormality. At lumbar puncture his CSF pressure was mildly elevated at 26 cm. The CSF contained 110 lymphocytes (normal less than 4), no polymorphs and no organisms on Gram staining. The CSF protein was mildly elevated at 0.6 g/dl and the CSF glucose level was a normal proportion of his blood glucose. As you will discover in Chapter 15, this CSF picture suggests intracranial infection, most likely viral encephalitis. He was treated with intravenous aciclovir. He subsequently had an MR brain scan which showed signal changes consistent with swelling and haemorrhage in both temporal and frontal lobes, typical of herpes simplex encephalitis. HSV was detected in his CSF using PCR. He rapidly improved but was left with persistent forgetfulness and occasional focal seizures. [стр. 276 ⇒]

Status epilepticus is a single prolonged seizure or a series of seizures without full recovery in between. Any type of seizure (convulsive or nonconvulsive) may appear under the guise of status epilepticus. In grand mal status epilepticus, patients do not regain consciousness between seizures. Location-related (focal, partial) epilepsy can be differentiated from generalized epilepsies and epileptic syndromes on the basis of the seizure pattern. Seizures that cannot be classified because of inadequate data on focal or generalized seizure development are called unclassified epilepsy or epileptic syndrome. Other terms used in classification refer to seizure etiology (e. g., idiopathic, cryptogenic, symptomatic). [стр. 205 ⇒]

If both of these medications fail to terminate the seizure, then the status epilepticus is considered refractory to medications. Continuous intravenous sedation is then required, and at this point, the patient must be intubated and mechanically ventilated. Many physicians advocate the use of fosphenytoin even if the initial status epilepticus has terminated, because the duration of efficacy of lorazepam is only 4–24 hours, possibly leaving patients with an increased risk of seizure recurrence. For refractory status epilepticus that has not responded to first- or second-line therapy, most epileptologists now advocate aggressive treatment with continuous intravenous sedation rather than intravenous valproate or intravenous phenobarbital, and the use of continuous EEG monitoring to... [стр. 77 ⇒]

Our interpretation There is insufficient data to support the routine use of steroids in HSE outside of the context of a randomized comparison against placebo. 4. Japanese encephalitis Do corticosteroids improve disability or mortality in adults or children with Japanese encephalitis? Japanese encephalitis (JE) is caused by the flavivirus JE virus. JE has grown as a problem in the last 50 years because of its geographical spread and increased incidence. There are approximately 50,000 cases and 15,000 deaths annually [45]. The clinical features of JE virus infection range from a nonspecific flu-like illness to a severe and often fatal meningoencephalomyelitis. JE typically presents after a few days of febrile illness, followed by headache, vomiting, and drowsiness often accompanied seizures. Extrapyramidal features may then set in [46]. Convulsions occur frequently in JE and are reported in up to 85% of children and 10% of adults [47]. Multiple or prolonged seizures and status epilepticus (especially subtle motor status epilepticus) are also associated with a poor prognosis [48]. A subgroup of JE patients presented with a polio-like acute flaccid paralysis presentation [49]. About 30% of hospitalized patients with JE die. Half the survivors have disabling neurological sequelae. Improvement in medical care may improve mortality rates but increase the number of patients with sequale [45] which include mixture of upper and lower motor neurone weakness, and cerebellar and extrapyramidal signs [50]. There is no specific antiviral treatment for JE. Nitric oxide, ribavirin, and interferon alpha have been effective in vitro or in animal models [51,52]. Interferon alpha has also been assessed in a randomized placebo controlled trial in humans but it did not improve the outcome [53]. Nursing care and physiotherapy are needed to reduce the risk of bedsores, malnutrition, and contractures. Symptomatic management of seizures and raised intracranial pressure are often needed. No systematic review was identified. One RCT was identified [54]. Sixty-five patients presenting in Thailand to four hospitals... [стр. 169 ⇒]

It occurs in a minority of patients with epilepsy and is more common in patients with an underlying structural cause than in patients with primary generalized epilepsy. It may be the first presentation of epilepsy. Status epilepticus may be precipitated by withdrawal of antiepileptic drugs or by intercurrent infection or may be spontaneous. Non-convulsive status epilepticus may be generalized (absence status) or focal/partial (complex partial or simple partial status). Convulsive status is a medical emergency and requires urgent and intensive treatment. Seizures which are multiple and frequent, but not continuous, may herald status and should be controlled rapidly. The principles of management of convulsive status epilepticus are: • simultaneous protection of airway and termination of seizure activity • prevention of further seizures • identification of cause of seizures. To stop the seizures use intravenous diazepam and, if this fails, intravenous clonazepam or intramuscular midazolam. All patients require urgent neuroimaging. In postoperative patients an urgent CT scan must be performed to exclude a postoperative collection, such as an intracerebral haemorrhage. Maintenance antiepileptic drug therapy should be introduced or optimized to prevent further seizures. [стр. 289 ⇒]

Thus, decreases in brain ATP and phosphocreatine concentrations become progressive, and the EEG discharges become self-sustaining. Irreparable injury may be the end result.5,61,68,76,77,109-118 Nevertheless, most studies indicate that the newborn brain is more resistant to seizure-induced neuronal necrosis than is the adult brain.94,119-125 Changes in high-energy phosphate compounds comparable to those observed in animal models were demonstrated by MR spectroscopy during subtle seizures in the human newborn (see Fig. 5-5).93 Prevention of the changes in high-energy phosphate levels that appear to be important in causation of brain injury by pharmacological treatment of seizure was shown by MR spectroscopy in the neonatal dog.92 Similarly, the immediately beneficial response to treatment of the seizure with phenobarbital also was demonstrated in the human newborn (Fig. 5-8).93 Work with newborn animals showed that glucose administration just before the seizures prevents the fall in brain glucose level that occurs with status epilepticus and markedly reduces mortality and brain cell loss.69,89 This protective effect of glucose was distinctly greater in newborn than in older animals (Fig. 5-9). The precise beneficial effect of the glucose did not seem to relate to brain ATP and phosphocreatine concentrations because neither concentration in whole brain was altered in these experiments. (Neuronal concentrations in selected brain regions could not be measured in this work.) The glucose did appear to serve as a carbon source, because DNA, RNA, protein, and cholesterol concentrations were relatively spared in the glucose-treated animals. In a study with potential clinical relevance, in which status epilepticus was induced in the neonatal rat subjected to hypoxia-ischemia,... [стр. 224 ⇒]

McDonald JW, Johnston MV, Young AB: Differential ontogenic development of three receptors comprising the NMDA receptor/channel complex in the rat hippocampus, Exp Neurol 110:237-247, 1990. 55. Cherubini E, Gaiarsa JL, Ben-Ari Y: GABA: An excitatory transmitter in early postnatal life, Trends Neurosci 14:515-519, 1991. 56. Moshé SL: Seizures in the developing brain, Neurology 43:S3-S7, 1993. 57. Moshe SL, Brown LL, Kubova H, Veliskova J, et al: Maturation and segregation of brain networks that modify seizures, Brain Res 665:141-146, 1994. 58. Moshe SL, Garant DS, Sperber EF, Veliskova J, et al: Ontogeny and topography of seizure regulation by the substantia nigra, Brain Dev 17:61-72, 1995. 59. Baram TZ, Snead OC 3rd: Bicuculline induced seizures in infant rats: Ontogeny of behavioral and electrocortical phenomena, Brain Res Dev Brain Res 57:291-295, 1990. 60. Sperber EF, Haas KZ, Stanton PK, Moshé SL: Resistance of the immature hippocampus to seizure-induced synaptic reorganization, Brain Res Dev Brain Res 60:88-93, 1991. 61. Jensen FE, Applegate CD, Holtzman D, Belin TR, et al: Epileptogenic effect of hypoxia in the immature rodent brain, Ann Neurol 29:629-637, 1991. 62. Romijn HJ, Voskuyl RA, Coenen AML: Hypoxic-ischemic encephalopathy sustained in early postnatal life may result in permanent epileptic activity and an altered cortical convulsive threshold in rat, Epilepsy Res 17:31-42, 1994. 63. Staley K, Smith R, Schaack J, Wilcox C, et al: Alteration of GABAA receptor function following gene transfer of the CLC-2 chloride channel, Neuron 17:543-551, 1996. 64. Yamada J, Okabe A, Toyoda H, Kilb W, et al: Cluptake promoting depolarizing GABA actions in immature rat neocortical neurones is mediated by NKCC1, J Physiol 557:829-841, 2004. 65. Clayton GH, Owens GC, Wolff JS, Smith RL: Ontogeny of cation-Clcotransporter expression in rat neocortex, Brain Res Dev Brain Res 109:281-292, 1998. 66. Rivera C, Voipio J, Payne JA, Ruusuvuori E, et al: The K+/Clco-transporter KCC2 renders GABA hyperpolarizing during neuronal maturation, Nature 397:251-255, 1999. 67. Dai Y, Tang J, Zhang JH: Role of Clin cerebral vascular tone and expression of Na+-K+-2Clco-transporter after neonatal hypoxia-ischemia, Can J Physiol Pharmacol 83:767-773, 2005. 68. Plum F, Howse DC, Duffy TE: Metabolic effects of seizures. In Plum F, editor: Brain Dysfunction in Metabolic Disorders, New York: 1974, Raven Press. 69. Dwyer BE, Wasterlain CG: Neonatal seizures in monkeys and rabbits: Brain glucose depletion in the face of normoglycemia, prevention by glucose loads, Pediatr Res 19:992-995, 1985. 70. Fujikawa DG, Vannucci RC, Dwyer BE, Wasterlain CG: Generalized seizures deplete brain energy reserves in normoxemic newborn monkeys, Brain Res 454:51-59, 1988. 71. Fujikawa DG, Dwyer BE, Lake RR, Wasterlain CG: Local cerebral glucose utilization during status epilepticus in newborn primates, Am J Physiol 256:C1160-1167, 1989. 72. Young RS, Cowan BE, Petroff OA, Novotny E, et al: In vivo 31P and in vitro 1H nuclear magnetic resonance study of hypoglycemia during neonatal seizure, Ann Neurol 22:622-628, 1987. 73. Cowan BE, Young RS, Briggs RW, Lu D, et al: The effect of hypotension on brain energy state during prolonged neonatal seizure, Pediatr Res 21:357-361, 1987. 74. Young RS, Petroff OA, Chen B, Gore JC, et al: Brain energy state and lactate metabolism during status epilepticus in the neonatal dog: In vivo 31P and 1H nuclear magnetic resonance study, Pediatr Res 29:191-195, 1991. 75. Young RS, Briggs RW, Yagel SK, Gorman I: 31P nuclear magnetic resonance study of the effect of hypoxemia on neonatal status epilepticus, Pediatr Res 20:581-586, 1986. 76. Wasterlain CG, Shirasaka Y: Seizures, brain damage and brain development, Brain Dev 16:279-295, 1994. 77. Wasterlain CG: Recurrent seizures in the developing brain are harmful, Epilepsia 38:728-734, 1997. 78. Thoresen M, Hallstrom A, Whitelaw A, Puka-Sundvall M, et al: Lactate and pyruvate changes in the cerebral gray and white matter during posthypoxic seizures in newborn pigs, Pediatr Res 44:746-754, 1998. 79. Lowry OH, Passonneau JV: Kinetic evidence for multiple binding sites on phosphofructokinase, J Biol Chem 241:2268-2279, 1966. 80. Borgstrom L, Chapman AG, Siesjö BK: Glucose consumption in the cerebral cortex of rat during bicuculline-induced status epilepticus, J Neurochem 27:971-973, 1976. 81. Lassen NA: Brain extracellular pH: The main factor controlling cerebral blood flow, Scand J Clin Lab Invest 22:247-251, 1968. 82. Young RS, Osbakken MD, Briggs RW, Yagel SK, et al: 31P NMR study of cerebral metabolism during prolonged seizures in the neonatal dog, Ann Neurol 18:14-20, 1985. 83. Fujikawa DG, Dwyer BE, Wasterlain CG: Preferential blood flow to brainstem during generalized seizures in the newborn marmoset monkey, Brain Res 397:61-72, 1986. 84. Clozel M, Daval JL, Monin P, Dubruc C, et al: Regional cerebral blood flow during bicuculline-induced seizures in the newborn piglet: Effect of phenobarbital, Dev Pharmacol Ther 8:189-199, 1985. 85. Young RS, Fripp RR, Yagel SK, Werner JC, et al: Cardiac dysfunction during status epilepticus in the neonatal pig, Ann Neurol 18:291-297, 1985. [стр. 253 ⇒]

Chapter 5 86. Pourcyrous M, Leffler CW, Bada HS, Korones SB, et al: Effects of pancuronium bromide on cerebral blood flow changes during seizures in newborn pigs, Pediatr Res 31:636-639, 1992. 87. Hascoet JM, Monin P, Vert P: Persistence of impaired autoregulation of cerebral blood flow in the postictal period in piglets, Epilepsia 29:743-747, 1988. 88. Monin P, Stonestreet BS, Oh W: Hyperventilation restores autoregulation of cerebral blood flow in postictal piglets, Pediatr Res 30:294-298, 1991. 89. Wasterlain CG, Duffy TE: Status epilepticus in immature rats, Arch Neurol 33:821, 1976. 90. Vannucci RC, Vasta F: Energy state of the brain in experimental neonatal status epilepticus, Pediatr Res 19:396, 1985. 91. Cataltepe O, Vannucci RC, Heitjan DF, Towfighi J: Effect of status epilepticus on hypoxic-ischemic brain damage in the immature rat, Pediatr Res 38:251-257, 1995. 92. Young RS, Chen B, Petroff OA, Gore JC, et al: The effect of diazepam on neonatal seizure: In vivo 31P and 1H NMR study, Pediatr Res 25:27-31, 1989. 93. Younkin D, Maris JE: The effect of seizures on cerebral metabolites in children, Pediatr Res 19:397, 1985. 94. Holmes GL: Effects of seizures on brain development: Lessons from the laboratory, Pediatr Neurol 33:1-11, 2005. 95. Wirrell EC, Armstrong EA, Osman LD, Yager JY: Prolonged seizures exacerbate perinatal hypoxic-ischemic brain damage, Pediatr Res 50:445-454, 2001. 96. Dzhala V, Ben-Ari Y, Khazipov R: Seizures accelerate anoxia-induced neuronal death in the neonatal rat hippocampus, Ann Neurol 48:632-640, 2000. 97. Yager JY, Armstrong EA, Jaharus C, Saucier DM, et al: Preventing hyperthermia decreases brain damage following neonatal hypoxic-ischemic seizures, Brain Research 1011:48-57, 2004. 98. Gado MH, Phelps ME, Hoffman EJ, Raichle ME: Changes in cerebral blood volume and vascular mean transit time during induced cerebral seizures, Radiology 121:105-109, 1976. 99. Kuhl DE, Engel J Jr, Phelps ME, Selin C: Epileptic patterns of local cerebral metabolism and perfusion in humans determined by emission computed tomography of 18FDG and 13NH3, Ann Neurol 8:348-360, 1980. 100. Perlman JM, Volpe JJ: Seizures in the preterm infant: Effects on cerebral blood flow velocity, intracranial pressure, and arterial blood pressure, J Pediatr 102:288-293, 1983. 101. Perlman JM, Herscovitch P, Kreusser KL, Raichle ME, et al: Positron emission tomography in the newborn: Effect of seizure on regional cerebral blood flow in an asphyxiated infant, Neurology 35:244-247, 1985. 102. Monin P, Clozel M, Morselli PL, Dubruc C, et al: Effect of seizures on brain phenobarbital concentration in newborn piglets, Epilepsia 28:179-183, 1987. 103. Borch K, Pryds O, Holm S, Lou H, et al: Regional cerebral blood flow during seizures in neonates, J Pediatr 132:431-435, 1998. 104. Alfonso I, Papazian O, Villalobos R, Acosta JI: Similar brain SPECT findings in subclinical and clinical seizures in two neonates with hemimegalencephaly, Pediatr Neurol 19:132-134, 1998. 105. Takei Y, Takashima S, Ohyu J, Takami T, et al: Effects of nitric oxide synthase inhibition on the cerebral circulation and brain damage during kainic acid–induced seizures in newborn rabbits, Brain Dev 21:253-259, 1999. 106. Boylan GB, Panerai RB, Rennie JM, Evans DH, et al: Cerebral blood flow velocity during neonatal seizures, Arch Dis Child Fetal Neonatal Ed 80:105110, 1999. 107. Eyre JA, Oozeer RC, Wilkinson AR: Continuous electroencephalographic recording to detect seizures in paralysed newborn babies, BMJ (Clin Res Ed) 286:1017-1018, 1983. 108. Lou HC, Friis HB: Arterial blood pressure elevations during motor activity and epileptic seizures in the newborn, Acta Paediatr Scand 68:803-806, 1979. 109. Meldrum B: Physiological changes during prolonged seizures and epileptic brain damage, Neuropadiatrie 9:203-212, 1978. 110. Lowenstein DH, Shimosaka S, So YT, Simon RP: The relationship between electrographic seizure activity and neuronal injury, Epilepsy Res 10:49-54, 1991. 111. Corsellis JA, Bruton CJ: Neuropathology of status epilepticus in humans. Adv Neurol 34:129-139, 1983. 112. Nevander G, Ingvar M, Auer R, Siesjö BK: Status epilepticus in well-oxygenated rats causes neuronal necrosis, Ann Neurol 18:281-290, 1985. 113. Meldrum B: Excitotoxicity and epileptic brain damage, Epilepsy Res 10:5561, 1991. 114. Meldrum BS: The role of glutamate in epilepsy and other CNS disorders, Neurology 44(Suppl 8):S14-S23, 1994. 115. Hussenet F, Boyet S, Nehlig A: Long-term metabolic effects of pentylenetetrazol-induced status epilepticus in the immature rat, Neuroscience 67:455-461, 1995. 116. Sankar R, Shin DH, Liu HT, Mazarati A, et al: Patterns of status epilepticus-induced neuronal injury during development and long-term consequences, J Neurosci 18:8382-8393, 1998. 117. Sankar R, Shin DH, Wasterlain CG: Serum neuron-specific enolase is a marker for neuronal damage following status epilepticus in the rat, Epilepsy Res 28:129-136, 1997. 118. Towfighi J, Housman C, Brucklacher R, Vannucci RC: Neuropathology of seizures in the immature rabbit, Dev Brain Res 152:143-152, 2004. 119. Nitecka L, Tremblay E, Charton G, Bouillot JP, et al: Maturation of kainic acid-brain damage syndrome in the rat. II. Histopathological sequela, Neurosci 13:1073-1094, 1984. 120. Holmes GL: The long-term effects of seizures on the developing brain: Clinical and laboratory issues, Brain Dev 13:393-409, 1991. [стр. 254 ⇒]

Fujikawa DG, Söderfeldt B, Wasterlain CG: Neuropathological changes during generalized seizures in newborn monkeys, Epilepsy Res 12:243251, 1992. 122. Sperber EF, Stanton PK, Haas K, Ackermann RF, et al: Developmental differences in the neurobiology of epileptic brain damage, Epilepsy Res Suppl 9:67-80, 1992. 123. Owens J, Robbins CA, Wenzel J, Schwartzkroin PA: Acute and chronic effects of hypoxia on the developing hippocampus, Ann Neurol 41:187-199, 1997. 124. Yang YL, Tandon P, Liu Z, Sarkisian MR, et al: Synaptic reorganization following kainic acid–induced seizures during development, Dev Brain Res 107:169-177, 1998. 125. Baram TZ: Long-term neuroplasticity and functional consequences of single versus recurrent early-life seizures, Ann Neurol 54:701-705, 2003. 126. Olney JW: Neurotoxicity of excitatory amino acids. In McGeer E, Olney JW, McGeer PL, editors: Kainic Acid as a Tool in Neurobiology, New York: 1978, Raven Press. 127. Ben-Ari Y, Tremblay E, Ottersen OP, Meldrum BS: The role of epileptic activity in hippocampal and ‘‘remote’’ cerebral lesions induced by kainic acid, Brain Res 191:79-97, 1980. 128. Ben-Ari Y, Cherubini E: Zinc and GABA in developing brain [letter], Nature 353:220, 1991. 129. Collins RC, Olney JW: Focal cortical seizures cause distant thalamic lesions, Science 218:177-179, 1982. 130. Collins RC, Lothman EW, Olney JW: Status epilepticus in the limbic system: Biochemical and pathological changes, Adv Neurol 34:277-288, 1983. 131. McDonald JW, Johnston MV: Physiological and pathophysiological roles of excitatory amino acids during central nervous system development, Brain Res Brain Res Rev 15:41-70, 1990. 132. Meldrum B: Protection against ischaemic neuronal damage by drugs acting on excitatory neurotransmission, Cerebrovasc Brain Metab Rev 2:27-57, 1990. 133. Meldrum B, Garthwaite J: Excitatory amino acid neurotoxicity and neurodegenerative disease, Trends Pharmacol Sci 11:379-387, 1990. 134. Clifford DB, Zorumski CF, Olney JW: Ketamine and MK-801 prevent degeneration of thalamic neurons induced by focal cortical seizures, Exp Neurol 105:272-279, 1989. 135. Furshpan EJ, Potter DD: Seizure-like activity and cellular damage in rat hippocampal neurons in cell culture, Neuron 3:199-207, 1989. 136. Millan MH, Chapman AG, Meldrum BS: Extracellular amino acid levels in hippocampus during pilocarpine-induced seizures, Epilepsy Res 14:139-148, 1993. 137. During MJ, Spencer DD: Extracellular hippocampal glutamate and spontaneous seizure in the conscious human brain, Lancet 341:1607-1610, 1993. 138. Chang D, Baram TZ: Status epilepticus results in reversible neuronal injury in infant rat hippocampus: Novel use of a marker, Dev Brain Res 77:133-136, 1994. 139. Koh S, Tibayan FD, Simpson JN, Jensen TE: NBQX or topiramate treatment after perinatal hypoxia-induced seizures prevents later increases in seizureinduced neuronal injury, Epilepsia 45:569-575, 2004. 139a. Cornejo BJ, Mesches MH, Coultrap S, Browning MD, et al: A single episode of neonatal seizures permanently alters glutamatergic synapses, Ann Neurol 61:411-426, 2007. 140. Mellits ED, Holden KR, Freeman JM: Neonatal seizures. II. A multivariate analysis of factors associated with outcome, Pediatrics 70:177-185, 1982. 141. Bergman I, Painter MJ, Hirsch RP, Crumrine PK, et al: Outcome in neonates with convulsions treated in an intensive care unit, Ann Neurol 14:642-647, 1983. 142. Painter MJ, Pippenger C, MacDonald H, Pitlick W: Phenobarbital and diphenylhydantoin levels in neonates with seizures, J Pediatr 92: 315-319, 1978. 143. Legido A, Clancy RR, Berman PH: Neurologic outcome after electroencephalographically proven neonatal seizures, Pediatrics 88:583-596, 1991. 144. Connell J, Oozeer R, de Vries L, Dubowitz LM, et al: Clinical and EEG response to anticonvulsants in neonatal seizures, Arch Dis Child 64:459464, 1989. 145. Connell J, Oozeer R, de Vries L, Dubowitz LM, et al: Continuous EEG monitoring of neonatal seizures: Diagnostic and prognostic considerations, Arch Dis Child 64:452-458, 1989. 146. McBride MC, Laroia N, Guillet R: Electrographic seizures in neonates correlate with poor neurodevelopmental outcome, Neurology 55:506-513, 2000. 147. Miller SP, Weiss J, Barnwell A, Ferriero DM, et al: Seizure-associated brain injury in term newborns with perinatal asphyxia, Neurology 58:542-548, 2002. 148. Sogawa Y, Monokoshi M, Silveira DC, Cha BH, et al: Timing of cognitive deficits following neonatal seizures: Relationship to histological changes in the hippocampus, Dev Brain Res 131:73-83, 2001. 149. Bo T, Jiang YW, Cao HY, Wang JM, et al: Long-term effects of seizures in neonatal rats on spatial learning ability and N-methyl-D-aspartate receptor expression in the brain, Dev Brain Res 152:137-142, 2004. 150. McCabe BK, Silveira DC, Cilio MR, Cha BH, et al: Reduced neurogenesis after neonatal seizures, J Neurosci 21:2094-2103, 2001. 151. Villeneuve N, Ben-Ari Y, Holmes GL, Gaiarsa J-L: Neonatal seizures induced persistent changes in intrinsic properties of CA1 rat hippocampal cells, Ann Neurol 47:729-738, 2000. 151a. Holmes GL, Ben-Ari Y: A single episode of neonatal seizures permanently alters glutamatergic synapses, Ann Neurol 61:379-381, 2007. 152. Volpe J: Neonatal seizures, N Engl J Med 289:413-416, 1973. [стр. 254 ⇒]

De Carolis MP, Muzii U, Romagnoli C, Zuppa AA, et al: Phenobarbital for treatment of seizures in preterm infant: A new administration scheme, Dev Pharmacol Ther 14:84-89, 1990. 417. Gal P, Toback J, Erkan NV, Boer HR: The influence of asphyxia on phenobarbital dosing requirements in neonates, Dev Pharmacol Ther 7:145-152, 1984. 418. Painter MJ, Scher MS, Stein AD, Armatti S, et al: Phenobarbital compared with phenytoin for the treatment of neonatal seizures, N Engl J Med 341:485-489, 1999. 419. Shirer AE: Fosphenytoin sodium (Cerebyx, Parke-Davis): Where will it fit in? In Question-of-the-Month, Westchester, NY: 1996, Drug Intelligence Center. 420. Morton LD, Rizkallah E, Pellock JM: New drug therapy for acute seizure management, Semin Pediatr Neurol 4:51-63, 1997. 421. Morton LD: Clinical experience with fosphenytoin in children, J Child Neurol 13:S19-S22, 1998. 422. Takeoka M, Krishamoorthy KS, Soman TB, Caviness vs: Fosphenytoin in infants, J Child Neurol 13:537-540, 1998. 423. Kriel RL, Cifuentes RF: Fosphenytoin in infants of extremely low birth weight, Pediatr Neurol 24:219-221, 2001. 424. Riviello JJ: Drug therapy for neonatal seizures. I, Pharmacol Rev 5:e215e220, 2004. 425. Lacey DJ, Singer WD, Horwitz SJ, Gilmore H: Lorazepam therapy of status epilepticus in children and adolescents, J Pediatr 108:771-774, 1986. 426. Giang DW, McBride MC: Lorazepam versus diazepam for the treatment of status epilepticus, Pediatr Neurol 4:358-361, 1988. 427. Crawford TO, Mitchell WG, Snodgrass SR: Lorazepam in childhood status epilepticus and serial seizures: Effectiveness and tachyphylaxis, Neurology 37:190-195, 1987. 428. Deshmukh A, Wittert W, Schnitzler E, Mangurten HH: Lorazepam in the treatment of refractory neonatal seizures: A pilot study, Am J Dis Child 140:1042-1044, 1986. 429. Maytal J, Novak GP, King KC: Lorazepam in the treatment of refractory neonatal seizures, J Child Neurol 6:319-323, 1991. 430. McDermott CA, Kowalczyk AL, Schnitzler ER, Mangurten HH, et al: Pharmacokinetics of lorazepam in critically ill neonates with seizures, J Pediatr 120:479-483, 1992. 431. Langslet A, Meberg A, Bredesen JE, Lunde PK: Plasma concentrations of diazepam and N-desmethyldiazepam in newborn infants after intravenous, intramuscular, rectal and oral administration, Acta Paediatr Scand 67:699-704, 1978. 432. Ramsey RE, Hammond EJ, Perchalski RJ, Wilder J: Brain uptake of phenytoin, phenobarbital, and diazepam, Arch Neurol 36:535, 1979. 433. Prensky AL, Raff MC, Moore MJ, Schwab RS: Intravenous diazepam in the treatment of prolonged seizure activity, N Engl J Med 276:779-784, 1967. 434. McMorris S, McWilliam PK: Status epilepticus in infants and young children treated with parenteral diazepam, Arch Dis Child 44:604-611, 1969. 435. Smith BT, Masotti RE: Intravenous diazepam in the treatment of prolonged seizure activity in neonates and infants, Dev Med Child Neurol 13:630-634, 1971. 436. Schiff D, Chan G, Stern L: Fixed drug combinations and the displacement of bilirubin from albumin, Pediatrics 48:139-141, 1971. 437. Nathenson G, Cohen MI, McNamara H: The effect of Na benzoate on serum bilirubin of the Gunn rat, J Pediatr 86:799-803, 1975. 438. Gamstorp I, Sedin G: Neonatal convulsions treated with continuous, intravenous infusion of diazepam, Ups J Med Sci 87:143-149, 1982. 439. Riviello JJ: Drug therapy for neonatal seizures. II, Pharmacol Rev 5:e262e268, 2004. 440. Sheth RD, Buckley DJ, Gutierrez AR, Gingold M, et al: Midazolam in the treatment of refractory neonatal seizures, Clin Neuropharmacol 19:165-170, 1996. 441. Castro Conde JR, Hernandez Borges AA, Martinez D, Campo CG, et al: Midazolam in neonatal seizures with no response to phenobarbital, Neurology 64:876-879, 2005. 441a. Yamamoto H, Aihara M, Niijima S, Yamanouchi H: Treatments with midazolam and lidocaine for status epilepticus in neonates, Brain Dev 29:559-564, 2007. 442. Hellström-Westas L, Westgren U, Rosén I, Svenningsen NW: Lidocaine for treatment of severe seizures in newborn infants. I. Clinical effects and cerebral electrical activity monitoring, Acta Paediatr Scand 77:79-84, 1988. 443. Hellström-Westas L, Svenningsen NW, Westgren U, Rosén I, et al: Lidocaine for treatment of severe seizures in newborn infants. II. Blood concentrations of lidocaine and metabolites during intravenous infusion, Acta Paediatr 81:35-39, 1992. 444. Radvanyi-Bouvet M-F, Torricelli A, Rey E, Bavoux F, et al: Effects of lidocaine on seizures in the neonatal period: Some electroclinical aspects. In Wasterlain CG, Vert P, editors: Neonatal Seizures, New York: 1990, Raven Press. 445. Boylan GB, Rennie JM, Chorley G, Pressler RM, et al: Second-line anticonvulsant treatment of neonatal seizures: A video-EEG monitoring study, Neurology 62:486-488, 2004. 446. Powell C, Painter MJ, Pippenger CE: Primidone therapy in refractory neonatal seizures, J Pediatr 105:651-654, 1984. [стр. 259 ⇒]

Tassinari CA, Bureau M, Dravet C, Dalla Bernardina B, Roger J. Epilepsy with continuous spikes and waves during sleep. In: Roger J, Dravet C, Bureau M, Dreifuss FE, Wolf P, eds. Epileptic syndromes in infancy, childhood and adolescence. London: John Libbey Eurotext, 1985; 194–204. Tassinari CA, Bureau M, Dravet C, Roget J, Daniele Natale O. Electrical status epilepticus during sleep in children (electrical status epilepticus of sleep). In: Sterman MB, Shouse MN, Passouant P, eds. Sleep and epilepsy. London: Academic Press, 1982; 465–479. [стр. 135 ⇒]

Duration Criteria: Acute: 1 month or less. Subacute: More than 1 month but less than 1 year. Chronic: 1 year or longer. Bibliography: Billard C, Autret A, Laffont F, Lucas B, Degiovanni E. Electrical status epilepticus during sleep in children: A reappraisal from eight new cases. In: Sterman MB, Shouse MN, Passouant P, eds. Sleep and epilepsy. London: Academic Press, 1982; 481–494. Dalla Bernardina B, Tassinari CA, Dravet C, Bureau M, Beghini G, Roger J. Epilepsie partielle benigne et etat de mal electroencephalographique pendant le sommeil. Rev Electroencephalogr Neurophysiol Clin 1978; 8: 350–353. Patry G, Lyagoubi S, Tassinari CA. Subclinical “electrical status epilepticus” induced by sleep in children. A clinical and electroencephalographic study of six cases. Arch Neurol 1971; 24: 242–252. [стр. 135 ⇒]

Barr J, Zomorodi K, Bertaccini EJ, et al: A double-blind, randomized comparison of i.v.lorazepam versus midazolam for sedation of ICU patients via a pharmacologic model. Anesthesiology2001; 95:286–298 20. Shafer A: Complications of sedation with midazolam in the intensive care unit and acomparison with other sedative regimens. Crit Care Med, 1998; 26:947–956. 21. Swart EL, Zuideveld KP, de Jongh J, et al: Population pharmacodynamicmodelling oflorazepam- and midazolam-induced sedation upon long-term continuous infusion in critically illpatients. Eur J ClinPharmacol, 2006; 62:185–194 22. Swart EL, de Jongh J, Zuideveld KP, et al: Population pharmacokinetics of lorazepam and midazolam and their metabolites in intensive care patients on continuous venovenous hemofiltration. Am J Kidney Dis2005; 45:360–371. 23. Swart EL, Zuideveld KP, de Jongh J, et al: Comparative population pharmacokinetics of lorazepam and midazolam during long-term continuous infusion in critically ill patients. Br J ClinPharmacol, 2004; 57:135–145 24. McKeage K, Perry CM: Propofol: A review of its use in intensive care sedation of adults. CNS Drugs 2003; 17:235–272 25. Carson SS, Kress JP, Rodgers JE, et al: A randomized trial of intermittent lorazepam versus propofol with daily interruption in mechanically ventilated patients. Crit Care Med2006; 34:1326–1332. 26. Barr J, Egan TD, Sandoval NF, et al: Propofol dosing regimens for ICU sedation based upon an integrated pharmacokinetic-pharmacodynamic model. Anesthesiology2001; 95:324–333 27. Riker RR, Fraser GL: Adverse events associated with sedatives, analgesics, and other drugs that provide patient comfort in the intensive care unit. Pharmacotherapy2005; 25(5 Pt2):8S–18S 28. Walder B, Tramèr MR, Seeck M: Seizure-like phenomena and propofol: A systematic review. Neurology2002; 58:1327–1332 29. Iyer VN, Hoel R, Rabinstein AA: Propofol infusion syndrome in patients with refractory status epilepticus: An 11-year clinical experience. Crit Care Med, 2009; 37:3024–3030 30. Parviainen I, Uusaro A, Kälviäinen R, et al: Propofol in the treatment of refractory status epilepticus. Intensive Care Med, 2006; 32:1075–1079 31. Voss LJ, Sleigh JW, Barnard JP, et al: The howling cortex: Seizures and general anesthetic drugs. AnesthAnalg. 2008; 107:1689–1703. Roberts RJ, 32. Barletta JF, Fong JJ, et al: Incidence of propofol-related infusion syndrome in critically ill adults: A prospective, multicenter study. Crit Care2009; 13:R169 33. Kam PC, Cardone D: Propofol infusion syndrome. Anaesthesia, 2007; 62:690–701 34. Ugur F., Gilcu N., Boyaci A. Intrathecal infusion therapy with dexmedetomidine supplemented morphine in cancer pain. ActaAnaeshesiol. Scand., 2007; 51: 388 35. Venn RM, Grounds RM: Comparison between dexmedetomidine and propofol for sedation in the intensive care unit: Patient and clinician perceptions. Br J Anaesth 2001; 87:684–690 36. Riker RR, Shehabi Y, Bokesch PM, et al; SEDCOM (Safety and Efficacy of Dexmedetomidine Compared With Midazolam) Study Group: Dexmedetomidine vs midazolam for sedation of critically ill patients: A randomized trial. JAMA 2009; 301:489–499 37. Shehabi Y, Ruettimann U, Adamson H, et al: Dexmedetomidine infusion for more than 24 hours in critically ill patients: Sedative and cardiovascular effects. Intensive Care Med 2004; 30:2188–2196 38. Pandharipande PP, Pun BT, Herr DL, et al: Effect of sedation with dexmedetomidine vs lorazepam on acute brain dysfunction in mechanically ventilated patients: The MENDS randomized controlled trial. JAMA 2007; 298:2644–2653]. [стр. 31 ⇒]

Status Epilepticus Status epilepticus is defined as more than 30 minutes of continuous seizure activity, or recurrent seizure activity without an intervening period of consciousness (6). The most common and potentially dangerous forms of status epilepticus are described below. 1. Generalized convulsive status epilepticus is the most common form of status epilepticus. Despite treatment, the mortality associated with this type of status epilepticus is 20%–27% (7,8). After about 30 minutes, generalized convulsive status epilepticus can degenerate to non-convulsive status (6). 2. Non-convulsive generalized status epilepticus (subtle status epilepticus) is associated with minimal or no motor activity and requires electroencephalography for diagnosis. As many as 25% of cases of status epilepticus are nonconvulsive (6), and this condition is responsible for 8% of cases of unexplained coma (9). In fact, the most common seizure recorded during electroencephalographic monitoring of patients with altered mental status is non-convulsive (10). Non-convulsive seizures are often refractory to therapy, and are associated with a 65% mortality (8). 3. Refractory status epilepticus is a seizure that lasts more than 1 or 2 hours or is refractory to therapy with 2 or 3 anticonvulsant agents (11). Almost one-third of cases of status epilepticus are refractory (11). 4. Myoclonic status epilepticus can occur in up to one-third of patients with persistent coma following out-of-hospital cardiac arrest. This condition is characterized by sound-induced or spontaneous irregular and repetitive movements of the face and extremities (12). When it persists for 24 hours following resuscitation, myoclonic status is a sign of devastating neurological damage ( 13). P.929... [стр. 988 ⇒]

Refractory Status Epilepticus Status epilepticus that is refractory to first and second line agents can be treated with infusions of propofol, midazolam, or pentobarbital (see Figure 51.1). Pentobarbital is the most effective of these agents but it often causes hypotension (21). Refractory cases require endotracheal intubation, mechanical ventilation, and electroencephalographic monitoring. A single dose of neuromuscular blocker may be required to facilitate intubation, but these agents can mask seizures, and EEG monitoring is recommended for continued neuromuscular blockade. [стр. 991 ⇒]

Status Epilepticus 6. Marik PE, Varon J. The management of status epilepticus. Chest 2004;126:582–591. Full TextBibliographic Links 7. Manno EM. New management strategies in the treatment of status epilepticus. Mayo Clin Proc 2003;78:508–518. Full TextBibliographic Links 8. Treiman DM, Meyers PD, Walton NY, et al. A comparison of four treatments for generalized convulsive status epilepticus: Veterans Affairs Status Epilepticus Cooperative Study Group. N Engl J Med 1998;339:792–798. Ovid Full TextBibliographic Links 9. Towne AR, Waterhouse EJ, Boggs JG, et al. Prevalence of nonconvulsive status epilepticus in comatose patients. Neurology 2000;54:340–345. Ovid Full TextBibliographic Links 10. Claassen J, Mayer SA, Kowalski RG, et al. Detection of electrographic seizures with continuous EEG monitoring in critically ill patients. Neurology 2004;62:1743–1748. Ovid Full TextBibliographic Links 11. Mayer SA, Claassen J, Lokin J, et al. Refractory status epilepticus: frequency, risk factors, and impact on outcome. Arch Neurol 2002;59:205–210. Ovid Full TextBibliographic Links 12. Wijdicks EF, Parisi JE, Sharbrough FW. Prognostic value of myoclonus status in comatose survivors of cardiac arrest. Ann Neurol 1994;35:239–243. Bibliographic Links 13. Morris HR, Howard RS, Brown P. Early myoclonic status and outcome after cardiorespiratory arrest. J Neurol Neurosurg Psychiatry 1998;64:267–268. Bibliographic Links 14. Bassin S, Smith TL, Bleck TP. Clinical review: status epilepticus. Crit Care 2002;6:137–142. Bibliographic Links... [стр. 1001 ⇒]

В редких случаях может развиться и настоящим status status epilepticus лишь у двух, причем у одного больного, наряду с алкоголизмом, в анамнезе имелась травма головного мозга. Течение алкогольной эпилепсии доброкачественное. Она не дает эпилептических изменений личности, слабоумия, сумеречных состояний и т. д. В случаях алкогольной эпилепсии прогноз благоприятный при условии абсолютного воздержания от алкоголя. Однако у лиц, продолжающих злоупотреблять алкоголем, припадки не прекращаются. Они появляются как в состоянии опьянения и похмелья, так и в трезвом виде. Припадки бывают редко, но протекают крайне тяжедо. С. Г. Жислин разделяет алкогольную эпилепсию на четыре группы: 1) алкогольные эпилептические припадки, которыми сопровождается белая горячка; 2) припадки, возникающие в состоянии опьянения или похмелья; 3) припадки, развивающиеся исключительно в состоянии похмелья; наряду с этим, отмечаются также припадки в светлые промежутки, вне всякой зависимости от приема алкоголя; эти случаи относятся к эпилептической болезни с доброкачественным течением; 4) случаи комбинации симптоматической эпилепсии при органическом поражении головного мозга с алкогольной интоксикацией. Однако настоящей алкогольной эпилепсией можно назвать лишь две первые группы, что подчеркивает также и С. Г. Ж ислин. Две другие формы эпилепсии представляют интерес лишь постольку, поскольку отражают влияние алкоголя на течение этих эпилепсий и являются иллюстрацией того, как добавочные вредные факторы в виде алкоголя провоцируют эпилепсию, находившуюся в латентном состоянии. Алкогольная эпилепсия характеризуется типичными эпилептиформными припадками, при которых часто можно проследить ауру, клонические и тонические судороги, прикусывание языка, недержание мочи и кала с последующими сном и амнезией. При сочетании алкогольной и других эпилепсий эпилептические симптомы сохраняются и после длительного воздержания от алкоголя, в то время как алкогольная эпилепсия при воздержании от алкоголя вскоре проходит. Братц по этому поводу категорически заявляет, что «никогда не бывает припадка, если больного на продолжительное время лишить алкоголя». Дифференциальный диагноз может представлять некоторые затруднения. Иногда доброкачественно протекающая эпилептическая болезнь может дать повод к смешению ее с алкогольной эпилепсией. В период злоупотребления алкоголем подобная эпилепсия может обостряться, в светлые же промежутки она переходит в латентную форму, почему и создается впечат192... [стр. 191 ⇒]

The majority of women (67%) do not experience a seizure in pregnancy.19 The seizure-free duration is the most important factor in assessing the risk of seizure deterioration.49 In Evidence women who were seizure free for at least 9 months to 1 year prior to pregnancy, 74–92% level 2– continued to be seizure free in pregnancy.49–51 The data from the EURAP (International Registry of Antiepileptic Drugs and Pregnancy) study showed that pregnant women with idiopathic generalised epilepsies were more likely to remain seizure free (74%) than those with focal epilepsies (60%).19 There is insufficient Evidence evidence to assess whether the rates of status epilepticus are increased in pregnant WWE level 2+ compared with nonpregnant women. Status epilepticus is defined as 30 minutes of continual seizure activity or a cluster of seizures without recovery. Currently, there are no tests to predict the risk of seizure deterioration in pregnancy. [стр. 14 ⇒]

Any seizure lasting more than 5 minutes is unusual and represents a high risk of progressing to convulsive status epilepticus, a life-threatening medical emergency which affects around Evidence 1% of pregnancies in WWE.82 Treatment should be initiated as soon as reasonably possible level 2– before status epilepticus and pharmacoresistance is established.83,84 Left lateral tilt should be established alongside maintenance of airway and oxygenation at all times. There are no studies on the optimal management of epileptic seizures in labour. Outwith pregnancy, benzodiazepines are the drug of choice in status epilepticus: ● In those with intravenous access, lorazepam given as an intravenous dose of 0.1 mg/kg (usually a 4 mg bolus, with a further dose after 10−20 minutes) is preferred. Diazepam 5–10 mg administered slowly intravenously is an alternative. ● If there is no intravenous access, diazepam 10−20 mg rectally repeated once 15 minutes later if there is a continued risk of status epilepticus, or midazolam 10 mg as a buccal preparation are suitable. If seizures are not controlled, consider administration of phenytoin or fosphenytoin. The loading dose of phenytoin is 10–15 mg/kg by intravenous infusion, with the usual dosage for Evidence an adult of about 1000 mg. Guidance on the management of seizures is available in the NICE level 2++ guideline on epilepsy.1 If there is persistent uterine hypertonus, consider administration of tocolytic agents. After the mother is stabilised, continuous electronic fetal monitoring should be commenced. If the fetal heart rate does not begin to recover within 5 minutes or if the seizures are recurrent, expedite delivery. This may require caesarean delivery if vaginal delivery is not imminent. The neonatal team should be informed, as there is a risk of neonatal withdrawal syndrome Evidence level 2– with the maternal use of benzodiazepines and AEDs.85... [стр. 21 ⇒]

Smith PE, Saunders J, Dawson A, Kerr MP. Intractable seizures in pregnancy. Lancet 1999;354:1522. Patsalos PN, Fröscher W, Pisani F, van Rijn CM. The importance of drug interactions in epilepsy therapy. Epilepsia 2002;43:365–85. Bardy A. Epilepsy and pregnancy: a prospective study of 154 pregnancies in epileptic women [thesis]. Helsinki, Finland, University of Helsinki; 1982. Pennell PB. EURAP outcomes for seizure control during pregnancy: useful and encouraging data. Epilepsy Curr 2006;6:186–8. Nei M, Daly S, Liporace J.A maternal complex partial seizure in labor can affect fetal heart rate. Neurology 1998;51:904–6. Schmidt D, Canger R, Avanzini G, Battino D, Cusi C, Beck-Mannagetta G, et al. Change of seizure frequency in pregnant epileptic women. J Neurol Neurosurg Psychiatry 1983;46:751–5. Kevat D, Mackillop L. Neurological diseases in pregnancy. J R Coll Physicians Edinb 2013;43:49–58. EURAP Study Group. Seizure control and treatment in pregnancy: observations from the EURAP epilepsy pregnancy registry. Neurology 2006;66:354–60. DeLorenzo RJ, Garnett LK, Towne AR, Waterhouse EJ, Boggs JG, Morton L, et al. Comparison of status epilepticus with prolonged seizure episodes lasting from 10 to 29 minutes. Epilepsia 1999;40:164–9. Alldredge BK, Gelb AM, Isaacs SM, Corry MD, Allen F, Ulrich S, et al. A comparison of lorazepam, diazepam, and placebo for the treatment of out-of-hospital status epilepticus. N Engl J Med 2001;345:631–7. McElhatton PR. The effects of benzodiazepine use during pregnancy and lactation. Reprod Toxicol 1994;8:461–75. Kuczkowski KM. Labor analgesia for the parturient with neurological disease: what does an obstetrician need to know? Arch Gynecol Obstet 2006;274:41–6. Daroff RB, Fenichel GM, Jankovic J, Mazziotta JC. Bradley’s Neurology in Clinical Practice. 6th ed. Philadelphia: Elsevier Saunders; 2012. Marinella MA. Meperidine-induced generalized seizures with normal renal function. South Med J 1997;90:556–8. Kuczkowski KM. Seizures on emergence from sevoflurane anaesthesia for Caesarean section in a healthy parturient. Anaesthesia 2002;57:1234–5. Hsieh SW, Lan KM, Luk HN, Jawan B. Postoperative seizures after sevoflurane anesthesia in a neonate. Acta Anaesthesiol Scand 2004;48:663. Kuczkowski KM. Sevoflurane and seizures: déjà vu. Acta Anaesthesiol Scand 2004;48:1216. Borthen I, Eide MG, Daltveit AK, Gilhus NE. Obstetric outcome in women with epilepsy: a hospital-based, retrospective study. BJOG 2011;118:956–65. Thomas SV, Syam U, Devi JS. Predictors of seizures during pregnancy in women with epilepsy. Epilepsia 2012;53: e85–8. Tran TA, Leppik IE, Blesi K, Sathanandan ST, Remmel R. Lamotrigine clearance during pregnancy. Neurology 2002;59:251–5. de Haan GJ, Edelbroek P, Segers J, Engelsman M, Lindhout D, Dévilé-Notschaele M, et al. Gestation-induced changes in lamotrigine pharmacokinetics: a monotherapy study. Neurology 2004;63:571–3. Chen L, Liu F, Yoshida S, Kaneko S. Is breast-feeding of infants advisable for epileptic mothers taking antiepileptic drugs? Psychiatry Clin Neurosci 2010;64:460–8. Davanzo R, Dal Bo S, Bua J, Copertino M, Zanelli E, Matarazzo L. Antiepileptic drugs and breastfeeding. Ital J Pediatr 2013;39:50. Meador KJ, Baker GA, Browning N, Clayton-Smith J, Combs-Cantrell DT, Cohen M, et al.; NEAD Study Group. [стр. 31 ⇒]

4.1 Status migrainosus Akhtar ND, Murray MA and Rothner AD. Status migrainosus in children and adolescents. Semin Pediatr Neurol 2001; 8: 27–33. Beltramone M and Donnet A. Status migrainosus and migraine aura status in a French tertiary-care center: An 11-year retrospective analysis. Cephalalgia 2014; 34: 633–637. Couch JR and Diamond S. Status migrainosus. Causative and therapeutic aspects. Headache 1983; 23: 94–101. Cure J and Rothrock J. Prolonged status migrainosus complicated by cerebellar infarction. Headache 2007; 47: 1091–1092. Gentile S, Rainero I, Daniele D, et al. Reversible MRI abnormalities in a patient with recurrent status migrainosus. Cephalalgia 2009; 29: 687–690. Lanfranconi S, Corti S, Bersano A, et al. Aphasic and visual aura with increased vasogenic leakage: an atypical migrainosus status. J Neurol Sci 2009; 285: 227–229. Perucca P, Terzaghi M and Manni R. Status epilepticus migrainosus: clinical, electrophysiologic, and imaging characteristics. Neurology 2010; 75: 373–374. Raskin NH. Treatment of status migrainosus: the American experience. Headache 1990; 30(Suppl 2): 550–553. [стр. 32 ⇒]

Лечение в последующие дни: · Больной продолжает прием лоразепама (мерлит, лорафен). При этом диазепам не используют. Лоразепам вводят перорально или через желудочный зонд в дозе 0,05-0,1 мг/кг два раза в сутки; · При отсутствии лоразепама используют карбамазепин (финлепсин, тегретол) 800-1200 мг/сут., разделенные на три приема; · Если ЭС купирован, оставляют наиболее эффективный противосудорожный препарат для базисной терапии, остальные препараты постепенно начинают отменять. · В последующие сутки уменьшить кратность введения препарата. Если нет противопоказаний, основной путь введения жидкости и нутриентов – энтеральный. Литература 1. J Stephen Huff. Status Epilepticus. Last Updated: March 28, 2005. http://www.emedicine.com/ 2. Карлов В.А., Андреева О.В. Применение инъекционного Депакина при лечении эпилептического статуса. РМЖ, Том 9 № 20, 2001. 3. Prasad A, Worrall BB, Bertram EH, Bleck TP: Propofol and midazolam in the treatment of refractory status epilepticus. Epilepsia 2001 Mar; 42(3): 380-6[... [стр. 47 ⇒]

Appleton, R., S. Macleod, and T. Martland, Drug management for acute tonic-clonic convulsions including convulsive status epilepticus in children. Cochrane Database Syst Rev, 2008(3): p. CD001905. 312. Yoong, M., R.F. Chin, and R.C. Scott, Management of convulsive status epilepticus in children. Arch Dis Child Educ Pract Ed, 2009. 94(1): p. 1-9. 313. www.palliativedrugs.com, Phenobarbital 2010. 314. Holmes, G.L. and J.J. Riviello, Jr., Midazolam and pentobarbital for refractory status epilepticus. Pediatr Neurol, 1999. 20(4): p. 259-64. 315. Osorio, I., R.C. Reed, and J.N. Peltzer, Refractory idiopathic absence status epilepticus: A probable paradoxical effect of phenytoin and carbamazepine. Epilepsia, 2000. 41(7): p. 887-94. 316. Bourgeois, B.F. and W.E. Dodson, Phenytoin elimination in newborns. Neurology, 1983. 33(2): p. 173-8. 317. Tudur Smith, C., A.G. Marson, and P.R. Williamson, Phenytoin versus valproate monotherapy for partial onset seizures and generalized onset tonic-clonic seizures. Cochrane Database Syst Rev, 2001(4): p. CD001769. 318. Tudur Smith, C., et al., Carbamazepine versus phenytoin monotherapy for epilepsy. Cochrane Database Syst Rev, 2002(2): p. CD001911. 319. McCleane, G.J., Intravenous infusion of phenytoin relieves neuropathic pain: a randomized, double-blinded, placebo-controlled, crossover study. Anesth Analg, 1999. 89(4): p. 985-8. 320. Mendoza, J., et al., Systematic review: the adverse effects of sodium phosphate enema. Aliment Pharmacol Ther, 2007. 26(1): p. 9-20. 321. Miles C, F.D., Goodman ML, Wilkinson SSM., Laxatives for the management of constipation in palliative care patients. The Cochrane Collaboration.; The Cochrane Library. 2009: JohnWiley&Sons, Ltd. 322. El-Tawil, S., et al., Quinine for muscle cramps. Cochrane Database Syst Rev, 2010(12): p. CD005044. 323. MHRA. Quinine: not to be used routinely for nocturnal leg cramps. 2010; Available from: http://www.mhra.gov.uk/Safetyinformation/DrugSafetyUpdate/CON085085. 324. Bell, S.G., Gastroesophageal reflux and histamine2 antagonists. Neonatal Netw, 2003. 22(2): p. 53-7. 435... [стр. 454 ⇒]

В остальные сроки механизм индукции был NMDA-зависимым, как и в контроле. В пилокарпиновой модели, во время латентной фазы, индукция пластичности была независимой от GluN2B-содержащих NMDA-рецепторов, а во время хронической фазы стала полностью NMDA-независимой. Полученные результаты свидетельствуют о возможном участие NMDA-независимых форм долговременной синаптической пластичности в эпилептогенезе. Работа поддержана грантом РНФ № 16-15-10202. Alterations of synaptic plasticity in the rat hippocampus after status epilepticus Zaitsev A.V.1,2*, Postnikova T.Y.1,2 1. Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS, SaintPetersburg, Russia; 2. Sechenov Institute of Evolutionary Physiology and Biochemistry; * aleksey_zaitsev@mail.ru Status epilepticus (SE), caused by various convulsants, can induce the development of epilepsy. In a pilocarpine model, almost all animals develop spontaneous seizures in a few weeks after SE, whereas in the pentylenetetrazole model, spontaneous convulsions are usually not observed. The mechanisms of epileptogenesis are diverse, including the alterations in synaptic plasticity. Electrophysiological studies show that after SE the characteristics of short-term and long-term synaptic plasticity can change. However, the mechanisms of these changes remain unclear. The study aimed to compare the characteristics of short-term and long-term synaptic plasticity in hippocampal slices after SE induced by pentylenetetrazole or pilocarpine. We examined synaptic plasticity immediately after SE (acute phase), during the first week (latent phase), and also after a month (chronic phase). We found changes in short-term plasticity (an increase in facilitation) only during the first day after pentylenetetrazole-induced SE. This result suggests a decrease in the probability of mediator release in the hippocampal synapses, which can be one of the mechanisms that prevent epileptogenesis. Long-term synaptic plasticity was weakened in both models at all time points tested. In the pentylenetetrazole model, the most significant deviations were found one day after SE, when the induction mechanism of long-term potentiation was disturbed. In the remaining periods, the induction mechanism was NMDA-dependent, as in control. In the pilocarpine model, during the latent phase, plasticity induction was independent of GluN2B-containing NMDA receptors, and during the chronic phase, it became entirely NMDA-independent. The obtained results indicate the possible participation of NMDA-independent forms of long-term synaptic plasticity in epileptogenesis. Supported by RSF project No. 16-15-10202. 55... [стр. 57 ⇒]

These changes occur regardless of the presence of EA in the cortex. 66. Нейрон-астроцитарные взаимодействтия в гиппокампе после status epilepticus Семьянов А.В.1,2* 1. Институт Биоорганической Химии РАН, Москва, Россия; 2. ННГУ им Лобачевского, Нижний Новгород, Россия; * semyanov@neuro.nnov.ru Epilepsy is a group of neurological disorders commonly associated with malfunction of neurons, that leads to their pathological synchronization and generation of seizures. Recent reports pointed to a possible contribution of astrocytes into this pathology. We used the lithium-pilocarpine model of status epilepticus (SE) in rats to monitor changes in astrocytes. Experiments were performed in hippocampal slices two weeks after SE induction, just before the onset of spontaneous seizures. Nissl staining revealed significant neurodegeneration in pyramidal cell layers of hippocampal CA1, CA3, and hilus, but not in granular cell layer of the dentate gyrus. A significant increase in density of astrocytes stained with astrocyte specific marker, sulforhodamine 101, was observed in CA1 stratum (str.) radiatum. The astrocytes in this area were also loaded with morphological tracer, Alexa Fluor 594, through patch pipette for two-photon imaging. Sholl analysis showed no changes in the size of the astrocytic domain or in the number of primary astrocytic branches, but significant reduction in the number of distal branches. Astrocytic branches resolved with diffraction-limited light microscopy are relatively thick and contain Ca2+ stores, such as mitochondria and endoplasmic reticulum. The atrophy of astrocytic branches correlated with reduced sizes of Ca2+ events, but not their overall frequency. Possible changes in volume fraction of unresolved perisynaptic astrocytic leaflets were assessed by comparing their fluorescent profile to the level of fluorescence in the soma. No significant differences between control and SE animals were detected. The results of spatial entropy-complexity spectrum analysis were also consistent with changes in ratio of astrocytic branches vs. leaflets. In addition, we observed uncoupling of astrocytes trough the gap-junctions, which was suggested as a mechanism for reduced K+ buffering. [стр. 117 ⇒]

Neuron-astrocyte interactions in hippocampus after status epilepticus Semyanov A.V.1,2* 1. Institute of Bioorganic Chemistry RAS, Moscow, Russia; 2. University of Nizhny Novgorod, Nizhny Novgorod, Russia; * semyanov@neuro.nnov.ru Epilepsy is a group of neurological disorders commonly associated with malfunction of neurons, that leads to their pathological synchronization and generation of seizures. Recent reports pointed to a possible contribution of astrocytes into this pathology. We used the lithium-pilocarpine model of status epilepticus (SE) in rats to monitor changes in astrocytes. Experiments were performed in hippocampal slices two weeks after SE induction, just before the onset of spontaneous seizures. Nissl staining revealed significant neurodegeneration in pyramidal cell layers of hippocampal CA1, CA3, and hilus, but not in granular cell layer of the dentate gyrus. A significant increase in density of astrocytes stained with astrocyte specific marker, sulforhodamine 101, was observed in CA1 stratum (str.) radiatum. The astrocytes in this area were also loaded with morphological tracer, Alexa Fluor 594, through patch pipette for two-photon imaging. Sholl analysis showed no changes in the size of the astrocytic domain or in the number of primary astrocytic branches, but significant reduction in the number of distal branches. Astrocytic branches resolved with diffraction-limited light microscopy are relatively thick and contain Ca2+ stores, such as mitochondria and endoplasmic reticulum. The atrophy of astrocytic branches correlated with reduced sizes of Ca2+ events, but not their overall frequency. Possible changes in volume fraction of unresolved perisynaptic astrocytic leaflets were assessed by comparing their fluorescent profile to the level of fluorescence in the soma. No significant differences between control and SE animals were detected. The results of spatial entropy-complexity spectrum analysis were also consistent with changes in ratio of astrocytic branches vs. leaflets. In addition, we observed uncoupling of astrocytes trough the gap-junctions, which was suggested as a mechanism for reduced K+ buffering. 67. Неонатальные введения липополисахарида влияют на поведение и экспрессию гена GluA1 в клетках гиппокампа взрослых крыс Зубарева О.Е.1*, Карепанов А.А.1, Дёмина А.В.1, Коваленко А.А.1, Ротов А.Ю.1 1. ФЕДЕРАЛЬНОЕ ГОСУДАРСТВЕННОЕ БЮДЖЕТНОЕ УЧРЕЖДЕНИЕ НАУКИ ИНСТИТУТ ЭВОЛЮЦИОННОЙ ФИЗИОЛОГИИ И БИОХИМИИ ИМ. И.М. СЕЧЕНОВА РОССИЙСКОЙ АКАДЕМИИ НАУК, С.-Петербург, Россия; * Зубарева О.Е.zubarevaoe@mail.ru Длительные когнитивные нарушения, появляющиеся уже в раннем возрасте, могут возникать не только под действием генетических особенностей, 116... [стр. 118 ⇒]

The role of nonlinearity in the formation of the rhythmic components of the spectrum of limbic structure electrical activity in guinea pig Bondar A.T.1,2*, Shubina L.V.1,2 1. Institute of Cell Biophysics of RAS, Pushchino, Russia; 2. Institute of Theoretical and Experimental Biophysics of Russian Academy of Sciences; * a_bond@rambler.ru Rhythmic electrical activity of nervous system is seen across a very broad range of frequencies, from 1 Hz, up to 100Hz. These frequencies do not represent a continuum, but have discrete levels: delta (1-4Hz), theta (4-8Hz), alpha (8-13Hz), beta (14-40Hz) and gamma (40-100Hz). In the literature there are few, but contradictory attempts to find a system (regularity) in the relationship of these rhythms. Our studies of local field potentials in guinea pig limbic structures during the development of status epilepticus revealed octave relationships of these rhythms with each other consisting in a cascade doubling of the dominating initial rhythm (1.8-2Hz) during the status epilepticus progression. It was shown that in addition to traditional rhythms under different functional states and loads, harmonic complexes representing Fourier series can be observed in the spectra of the electrical activity of brain structures. In the present study, we consider the mechanisms of formation of these complexes, as well as their functional role. The following classification is proposed: 1) the first type is harmonics associated with the non-linear nature of the evoked electrical activity in response to rhythmic photostimulation. These harmonics represent independent processes; they are spatially separated and have different functional purposes; 2) the second type is harmonics arising during epileptic paroxysms. In this case, the harmonics are an epiphenomenon, they are not independent processes, but reflect the form of a periodic sharp-wave process. It is assumed that these two types of spectrum components are formed in recurrent nerve networks that perform elementary nonlinear operation of amplitude modulation of incoming rhythmic signals by recurrent rhythms returning through feedbacks. The neurodynamics of such networks is iterative, which determines their unusual properties. Supported by the RFBR (NNo. 16-34-00457, 17-44-500312, 18-015-00157) and RHSF (No. 16-06-00133). [стр. 155 ⇒]

The seizures were induced in 3-week-old rats by injections of LiCl 127 mg/kg, i.p., and 24 h later methylscopolamine 1 mg/kg, i.p. and pilocarpine 30 mg/kg, i.p. Field EPSPs (fEPSPs) were evoked in CA1 of hippocampal slice. LTP was induced with theta-burst protocol. To evaluate the role of GluN2B-containing NMDA receptors their selective antagonist ifenprodil (3 mM) was used. During the first week after status epilepticus, we observed the significant reduction of hippocampal LTP. In the control group, the amplitude of response after the stimulus protocol was 155 ± 7% of baseline (n = 13), while in the experimental group LTP was smaller (130 ± 4%, n = 12, p <0.01). In the presence of ifenprodil, LTP was significantly reduced in control group (115 ± 5%, n = 8), while it was less affected in the experimental rats (123 ± 11%, n = 5). Assessment of mRNA expression of GluN2A, GluN2B, as well as the ratio of GluN2B/GluN2A in the hippocampus of control and experimental animals after status epilepticus showed reduction of GluN2B expression (t = 2.45, p = 0.03). These results indicate that GluN2B-containing NMDA receptors play an important role in the LTP formation; their decreased expression may reduce LTP in hippocampus. This work was supported by grants of RFBR 15-04-02951 and № 3-04-00244... [стр. 52 ⇒]

Role of glutamatergic systems in epilepsy Zaitsev A.V.1* 1. Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS, Saint-Petersburg, Russia; * aleksey_zaitsev@mail.ru Epilepsy - is a heterogeneous disease, and it is caused by a genetic predisposition (idiopathic epilepsy), or by a brain injury, stroke, hypoxia, infections, tumors (secondary or symptomatic epilepsy). The pathophysiology of epilepsy is that seizures result from imbalance between inhibitory (GABAergic) and excitatory (glutamatergic) mediatory systems in various regions of the brain. Based on experimental studies of animal models of epilepsy, as well as the studies of human epileptic brain it was reported a number of disturbances in glutamatergic and GABAergic systems. However, the data about specific changes in neurotransmitter systems are contradictory due to the heterogeneity of the disease and the use of different experimental approaches. In our work, we used different animal models of epilepsy (pilocarpine- and pentylenetetrazole-induced seizures, MES-test and Krushinsky-Molodkina audiogenic seizure-susceptible rats) to investigate the role of glutamatergic system. We found that specific blockers of NMDA or AMPA glutamate receptors have different effects on convulsions and their efficacy depends on the type of seizure model. Using real-time PCR and electrophysiological experiments on isolated neurons and slices of hippocampus and cortex we found that status epilepticus induced by systemic administration of pilocarpine leads to changes in the subunit composition of AMPA and NMDA receptors in the cortex and hippocampus of rats. In particular, we revealed that after status epilepticus pyramidal cells of the cerebral cortex begin to express calcium-permeable AMPA receptors which are normally absent. Changes in the NMDA receptor subunit composition are accompanied by disturbances in the long-term synaptic plasticity in hippocampal slices. These results provide new ideas for developing new effective antiepileptic drugs. This work was supported by the grants of RFBR 13-04-00244, 14-04-00413 and 15-04-02951... [стр. 58 ⇒]

...lu@gmail.com Glutamatergic neurotoxicity may result in delayed damage of the brain and development of epilepsy. Glutamate receptor agonist kainic acid (KA) is a potent neurotoxin and it is exploited in the modeling of epilepsy in animals. Endocannabinoids (eCB) have been shown to possess anticonvulsant properties in vivo. Modulation of cannabinoid signaling through the inhibition of EC inactivation may be an alternative and more physiological way than direct activation with CB1 receptor agonists. To address this problem we investigated the effects of the eCB reuptake inhibitor AM404, inhibitor of the enzymatic degradation of eCB anandamide URB597 and CB1 receptor antagonist AM251 on the KA-induced status epilepticus in guinea pigs. Local field potentials were recorded simultaneously in the hippocampus, entorhinal cortex, medial septum and amygdala before (3-4 days), during (4-6 hours) and after (3 months) the injection of KA. Within three months after the KA injection complex dynamic of changes in the electrical activity of the investigated brain structures was observed, while in the hippocampus the power of oscillations was significantly increased in one month after the KA administration. Moreover, in three months after the KA injection, along or with the AM251, cell loss and mossy fiber sprouting were detected in the dorsal hippocampus. Inhibition of eCB inactivation alleviated the severity of status epilepticus, prevented epileptogenesis and morphological alterations in the dorsal hippocampus, pointing out the potential possibility of the eCB system activation for treatment of epilepsy and other neurodegenerative diseases. Supported by the RFBR (№15-04-05463_а, №14-44-03607 р_центр_а). [стр. 61 ⇒]

...lu@gmail.com Endocannabinoids (EC) have been shown to possess anticonvulsant properties in vivo. Modulation of cannabinoid signaling through the inhibition of EC transport may be an alternative and more physiological way than direct activation with CB receptor agonists. To address this problem we investigated the effects of an inhibitor of the enzymatic degradation of the endocannabinoid anandamide (fatty acid amide hydrolase inhibitor, URB597, 4.8 nmol) on the kainic acid-induced SE (KA, 2 nmol, i.c.v.) in waking guinea pigs. Intrabrain EEGs were recorded simultaneously in hippocampus, entorhinal cortex, medial septal region, and amygdala before (3-4 days), during (4-6 hours) and after (3 months) the SE. KA administration induced sustained limbic seizures (status epilepticus) lasting for several hours. After several months in this group of guinea pigs spontaneous high frequency/amplitude EEG activities and mossy fiber sprouting were observed. In addition increase in EEG power of different hippocampal frequency bands and of high frequency band (120-300Hz) of all recorded structures were detected. When URB597 was injected immediately before KA, the seizure scores were markedly reduced although the electrographic seizures were sometimes registered. Also there were neither spontaneous seizure activities nor mossy fiber sprouting in this group of animals. These results suggest that the enzyme of endocannabinoids degradation can be targeted pharmacologically to modulate seizure severity and its inhibition can mediate neuroprotection in the КА-induced status epilepticus model of temporal lobe epilepsy. Supported by The Grant of the President of Russian Federation №3796.2012.4, The Scientific School (Grant №850.2012.4), RFBR №12-04-00776-а. [стр. 82 ⇒]

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