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Electrocerebral recovery during the intracarotid amobarbital procedure: influence of interval between injections allergy forecast okc buy clarinex now. Memory assessment during the intracarotid amobarbital procedure: influence of injection order allergy symptoms in horses discount clarinex 5mg fast delivery. Independent recovery of memory and language functioning during the intracarotid sodium amytal test allergy home generic 5 mg clarinex otc. Reduced anesthetization during the intracarotid amobarbital (Wada) test in patients taking carbonic anhydrase-inhibiting medications. Selective posterior cerebral artery Amytal test for evaluating memory function before surgery for temporal lobe seizure. Selective posterior cerebral artery injection of amytal: new method of preoperative memory testing. The utility of the intracarotid Amytal procedure in determining hemispheric speech lateralization in pediatric epilepsy patients undergoing surgery. Factors in children that predict performance on the intracarotid amobarbital procedure. Prediction of verbal memory decline after epilepsy surgery in children: effectiveness of Wada memory asymmetries. Wada memory asymmetry scores and postoperative memory outcome in left temporal epilepsy. Effect of Wada methodology in predicting lateralized memory impairment in pediatric epilepsy surgery candidates. Hippocampal memory function as reflected by the intracarotid sodium methohexital Wada test. Medial temporal and prefrontal contributions to working memory tasks with novel and familiar stimuli. Beyond speech lateralization: a review of the variability, reliability, and validity of the intracarotid amobarbital procedure and its nonlanguage uses in epilepsy surgery candidates. Objective criteria for reporting language dominance by intracarotid amobarbital procedure. Mixed speech dominance in the Intracarotid Sodium Amytal Procedure: validity and criteria issues. An update on determination of language dominance in screening for epilepsy surgery: the Wada test and newer noninvasive alternatives. Intracarotid amobarbital procedure as a predictor of material-specific memory change after anterior temporal lobectomy. Memory performance during the intracarotid amobarbital procedure and neuropsychological assessment in medial temporal lobe epilepsy: the limits of material specificity. Predictors of outcome after anterior temporal lobectomy: the intracarotid amobarbital test. Wada memory performance predicts seizure outcome following anterior temporal lobectomy. Predictors of outcome after temporal lobectomy for refractory temporal lobe epilepsy. Use of the intracarotid amobarbital procedure in the lateralization of the epileptogenic zone. Correlation of criteria used for localizing epileptic foci in patients considered for surgical therapy of epilepsy. The Wada test in Austrian, Dutch, German, and Swiss epilepsy centers from 2000 to 2005: a review of 1421 procedures. The role of the Wada test in the surgical treatment of temporal lobe epilepsy: an international survey. The role of the intracarotid amobarbital procedure in evaluation of patients for epilepsy surgery. A test for separating secondary from primary bilateral synchrony in epileptic subjects. Post operative amnesia after "passing" memory testing during the intracarotid amobarbital procedure. Effect of Wada memory stimulus type in discriminating lateralized temporal lobe impairment. Evidence-based practice: a reevaluation of the intracarotid amobarbital procedure (Wada test). The role of the Wada test in the surgical treatment of temporal lobe epilepsy: an international perspectivecommentary on Baxendale, et al.
The clinical diagnosis of "neonatal seizures" was independently and significantly associated with these adverse outcomes and eclipsed only by "intracranial hemorrhage" in forecasting them allergy tcm treatment purchase clarinex 5mg with mastercard. Neurologic functioning may even be impaired in those who appear "normal" after neonatal seizures (24) allergy symptoms with cough purchase clarinex 5mg with amex. Outcome has been assessed in terms of survival allergy symptoms from eggs order genuine clarinex, neurologic disability, developmental delay, and postnatal epilepsy. Ortibus and colleagues (25) reported that 28% died; 22% of survivors were neurologically normal at an average of 17 months of age; 14% had mild abnormalities; and 36% were severely abnormal. The mortality rate was 19% with a favorable outcome found in only 34% of patients. Cerebral palsy was identified in 37%, developmental delay in 34%, and 21% had postnatal epilepsy at 24 months of follow-up. Preliminary results of the Neonatal Seizures Clinical Research Centers from 1992 to 1997 have been reported (27). Whether seizures themselves adversely affect the developing brain is difficult to determine from clinical studies. Seizure burden may appear to influence outcome because some infants who experience brief, infrequent seizures may have relatively good long-term outcomes, whereas those with prolonged seizures often do not fare as well. Overall neurologic outcome was more favorable in those with two or fewer seizures per hour than in those with more than that number. In the subgroup with seizures caused by asphyxia, cerebral palsy was more frequent when more than five seizures occurred per hour. However, these results might equally reflect more severe underlying injuries that triggered both the additional short-term seizures and greater morbidity on long-term follow-up. Attempting a balanced approach, McBride and coworkers (29) followed up 68 high-risk neonates with birth asphyxia, meningitis, and other stressors linked to neonatal seizures. Based on logistic regression analysis, electrographic neonatal seizures were significantly correlated with death and cerebral palsy. One study found that patients with neonatal status epilepticus were at a higher risk for severe neurologic disability and postnatal epilepsy than those with fewer seizures (22). Neonatal Seizures May Be Inherently Harmful Neonatal seizures may be intrinsically harmful to the brain (31). Most seizures were long assumed to be the innocuous, albeit conspicuous, result of an acute injury, and the subsequent long-term neurodevelopmental abnormalities the result of their underlying causes, not the seizures themselves. Basic laboratory studies focused on the effects of seizures on the developing brain have not resolved the controversy (3236). Immature animals are more resistant than older animals to some seizure-induced injury (37). The immature brain may be resistant to acute seizure-induced cell loss (34); however, functional abnormalities such as impairment of visualspatial memory and reduced seizure threshold (38) occur after seizures, and seizures have been noted to induce changes in brain development, including altered neurogenesis (39), synaptogenesis, synaptic pruning, neuronal migration, and the sequential expression of genes including neurotransmitter receptors and transporters (40,41). While neonatal seizures seem to induce little histologic damage to the brain (37), studies have revealed that recurrent seizures can produce long-lasting changes in the developing brain, making them more prone to epilepsy and impairing future learning and behavior. Alterations in receptor subunit expression have been implicated as a cause for some of the changes following neonatal seizures. A recent study demonstrated that a single episode of seizures in neonatal rat pups (at P7) produced long-lasting alterations in excitatory glutametergic synapses that impaired working memory in adulthood (44). The most frequent clinical setting for the occurrence of neonatal seizures in both term and preterm neonates is following hypoxicischemic injury (20). A rodent study of hypoxiainduced seizures demonstrated a decrease in GluR2 receptor expression allowing an increase in calcium influx that may contribute to the chronic epileptogenic effects of hypoxiainduced neonatal seizures (46). These studies highlight the potential utility of topiramate in neonates with seizures associated with hypoxicischemic encephalopathy, but the lack of an intravenous formulation makes treatment in critically ill children challenging (49). A concern with recurrent neonatal seizures is the concept that "seizures beget seizures"-with recurrent seizures inducing secondary ictal onset zones. They dissected two intact neonatal hippocampi with their connecting commissural fibers and placed them in three contiguous chambers. Recurrent seizures were induced in one hippocampus with repeated doses of kainate that eventually propagated to the other hippocampus and established a secondary epileptogenic focus.
These electrodes are preferred for nocturnal recordings because of the artifact generated by eye movement and blinking (2) allergy hot flashes purchase 5 mg clarinex with visa. In frontal lobe epilepsy allergy symptoms at night generic clarinex 5 mg mastercard, seizures may begin in the dorsolateral frontal cortex allergy medicine you can take with alcohol order clarinex cheap, orbitofrontal region, cingulate gyrus, supplementary cortex, or frontal pole (7). Interictal frontal lobe epileptogenic discharges may be associated with simple partial, complex partial, atonic, or secondarily generalized tonicclonic seizures (5,12). Ictal behavior in frontal lobe epilepsy is highly variable, and establishing the diagnosis based on ictal semiology alone may be difficult (7). Frontal lobe seizures, especially those arising from the supplementary sensorimotor region, may be confused with nonepileptic behavioral events (7). Perirolandic Epilepsy the most common cause of perirolandic epilepsy is benign childhood epilepsy with centrotemporal spikes, or "rolandic epilepsy. The central midtemporal spike-wave may exhibit a surrounding region of positivity, suggesting a tangential dipole source (3,5). The discharges may be unilateral or bilateral, shift from side to side, and may not correspond to the hemisphere associated with ictal symptoms (5). Spiking is usually more abundant during drowsiness and sleep and is not a good predictor of the severity of seizure activity. Central spikes-waves have a moderate degree of epileptogenicity, with approximately 40% to 60% of patients having clinical seizures (5). Seizure onset is typically between 2 and 12 years of age, and seizures disappear between 15 and 18 years of age (39). Antiepileptic drug therapy can usually be deferred, although the seizures typically respond well if treatment is elected. The ictal behavior includes focal motor or sensory seizures with frequent secondary generalization, excessive salivation and drooling, and motor speech arrest (40). Hyperventilation, hypoglycemia, drowsiness, and eye closure may potentiate the generalized spike-wave discharge (41). During sleep, the morphology of the interictal abnormality may appear as fragmented or asymmetric spike-wave bursts (41). However, some intermittent, rhythmic, bisynchronous slow waves may be present over the posterior head regions (41). This highly epileptogenic pattern occurs typically in children 3 to 15 years old with idiopathic generalized epilepsy and absence seizures (41). Seizure types include absence, generalized tonicclonic, atonic, myoclonic, tonic, clonictonicclonic, and atypical absence (40). Electrographic correlate of a typical absence seizure precipitated by hyperventilation. Response testing during the seizure shows that the patient stopped pressing the button when a clicking sound was made in his ear. They usually occur frequently (multiple daily) as brief absences that typically last less than 30 seconds. Multiple Spike and Wave the multiple spike-and-wave pattern (also called atypical spike and wave and fast spike and wave) consists of a generalized mixture of intermittent brief spike and polyspike complexes associated with slow waves of variable frequency (3. The background between bursts may be normal or contain focal or generalized slow irregularities. This pattern is associated with generalized tonicclonic, clonic, atonic, myoclonic, and atypical absence seizures (24). The tonic phase begins with generalized, low-voltage, fast activity (the "epileptic recruiting rhythm") that progresses to a generalized spike and polyspike burst. Postictally, at the termination of the seizure, prominent generalized background slowing gradually returns to baseline. Often, no clinical manifestations are apparent, although appropriate testing may disclose some alteration in psychomotor performance. Focal spikes and focal or generalized background slowing between the spike-wave bursts may also be present (44).
Neuromagnetic assessment of epileptogenicity in cerebral arteriovenous malformation allergy medicine without decongestant order clarinex canada. Source localization and possible causes of interictal epileptic activity in tumor-associated epilepsy allergy on lips cheap 5 mg clarinex with visa. Postoperative multichannel magnetoencephalography in patients with recurrent seizures after epilepsy surgery allergy testing emedicine purchase genuine clarinex online. Source localization of mesial temporal interictal epileptiform discharges: correlation with intracranial foramen ovale electrodes. Concordance between routine interictal magnetoencephalography and simultaneous scalp electroencephalography in a sample of patients with epilepsy. Utilization of magnetoencephalography results to obtain favourable outcomes in epilepsy surgery. Magnetoencephalography/magnetic source imaging in the assessment of patients with epilepsy. Clonidine and methohexitalinduced epileptic magnetoencephalographic discharge in patients with focal epilepsies. Magnetic brain source imaging of focal epileptic activity: a synopsis of 455 cases. Magnetoencephalographic patterns of epileptiform activity in children with regressive autism spectrum disorders. Detecting possible underlying structural abnormalities or causes of epilepsy is one important aspect of such advances, and currently pathologic lesions are identified in about 80% of all refractory focal epilepsies (2). In addition, novel imaging results are being explored to inform about cortical function or dysfunction in patients with epilepsy, as well as correlates of the ictal-onset zone and irritative zone (3). The objective of epilepsy surgery in pharmacoresistant focal epilepsies is the complete resection or at least disconnection of the epileptogenic zone while preserving eloquent cortex (2,4). This chapter focuses on the contribution of two novel imaging technologies to optimize surgical results. In addition, white matter architecture and tract morphology can be interrogated allowing for the first time to reconstruct major tracts in vivo. Together, both technologies may allow for novel insights in understanding the ictal-onset zone, irritative zone, and functional deficit zone. Taking measurements in at least three directions allows for characterization of the mean diffusion properties within a voxel in the image. By applying diffusion gradients in six or more directions, the diffusion tensor, a mathematical construct, can be calculated. This allows assessing not only the amplitude of diffusional motion, but also the directionality (1315). The fact that diffusion is not the same in the three main spatial directions, but is asymmetric in the brain and restricted in certain directions, gave rise to the concept of "anisotropy" (13,16). Diffusion in different directions, such as parallel (main direction of diffusion) and perpendicular to the main fiber tract orientation, can be studied. Together, these quantitative measures help to characterize the integrity of the underlying white matter and may allow understanding of the pathophysiologic mechanisms consistent with such diffusion abnormalities. Exploring white matter changes in epilepsy, how they relate to epileptogenicity, and whether they may be a surrogate marker for cognitive difficulties is a matter of ongoing research. In a medium without any boundaries, the random translational motion or Brownian motion of water molecules results from the thermal energy carried by these molecules. In the brain, however, such diffusion is restricted by intra- and extracellular boundaries. Using an in vitro model of Wallerian degeneration in frog sciatic nerve, axonal and myelin degeneration causes a decrease in diffusion anisotropy due to reduced parallel and increased perpendicular diffusivity (9). Myelin has been shown to modulate perpendicular diffusivity (7,8), although it is not the only factor involved (17). In humans, reductions in the principal direction and increases in radial diffusivities have been shown in chronically degenerated 877 878 Part V: Epilepsy Surgery white matter tracts (18). An initial decrease in parallel diffusivities evidencing the breakdown of the axons (19,20) is followed in the chronic stage (2 to 4 months later) by an increase of the radial diffusivities as myelin sheath degeneration is noted. Water molecules become more mobile perpendicular to the axons, resulting in an increase in radial diffusivities. Tractography Lastly, anisotropy information forms the basis of reconstructing tracts.
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