1,721,074 research outputs found
Antiepileptic drugs as a cause of worsening of seizures.
No full textPURPOSE: Although the paradoxical ability of antiepileptic drugs (AEDs) to increase seizure activity has been recognized for decades, the underlying mechanisms are poorly understood and few systematic studies have addressed this problem. This article is intended to provide a critical review of available literature on this topic.
METHODS: Information was collected by means of computerized literature searches, screening of journals and textbooks, and consultation with colleagues. Mechanisms which potentially might precipitate underlying drug-induced exacerbation of seizures were considered based on available pharmacologic and clinical knowledge.
RESULTS: The reviewed information suggests that a paradoxical increase in seizure frequency may occur as a result of at least two separate mechanisms. The first appears to involve a nonspecific manifestation of drug intoxication; seizure-worsening in this context is usually reversible by dosage reduction or elimination of unnecessary polypharmacy. Conversely, the other mechanism may involve a distinct adverse primary action of the drug in specific seizure types or in syndromic forms. Carabamazepine, in particular, has been reported to precipitate or exacerbate a variety of seizures, most notably absence, atonic, or myoclonic seizures in patients with generalized epilepsies characterized by bursts of diffuse and bilaterally synchronous spike-and-wave EEG activity. Phenytoin and vigabatrin also have been implicated in worsening of seizures, particularly generalized seizures, whereas gabapentin has been associated repeatedly with precipitation of myoclonic jerks. Benzodiazepines occasionally have been reported to precipitate tonic seizures, especially when given intravenously to control other seizure types in patients with Lennox-Gastaut syndrome. Seizure deterioration has been reported also with other drugs; though in most cases evidence is still insufficient for meaningful conclusions to be drawn.
CONCLUSIONS: Drug-induced exacerbation of seizures is a serious and common clinical problem that is often unrecognized or overlooked by the treating physician. Its occurrence appears to be related to three possible causes: an incorrect diagnosis of seizure type or syndromic form, lack of knowledge about certain drugs that are contraindicated in specific types of epilepsies, or to prescription of excessive drug dosages and drug combinations. Further studies are required to evaluate the prevalence of this phenomenon of drug-induced exacerbation of seizures, to investigate its mechanisms in greater detail and to characterize additional prognostic factors that may be used for early identification of patients at risk
Infantile spasms in Down syndrome - Effects of delayed anticonvulsive treatment
No full textTo investigate the impact of treatment lag in infantile spasms (IS) on treatment response, occurrence of later epilepsy, and long-term cognition and behavior in patients with one single etiological entity, we examined 18 patients with Down syndrome (DS) and earlier IS retrospectively (follow-up period of 32-180 months with a mean of 85.1 months), and determined their history and present condition, in terms of previously mentioned items. There was a statistically significant correlation between treatment lag and lag to cessation of spasms (R = 0.55, P = 0.02), developmental quotient (DQ) (R = -0.75, P = 0.003), and score of autistic features (AF) (R = 0.57, P = 0.04). Moreover we found that the later the response to treatment of IS, the lower was the DQ (R = -0.86, P = 0.001) and the higher was the score of autistic features (R = 0.5, P = 0.06). A long duration of spasms also determined a low DQ (R = -0.93, P < 0.0001) and a high score of autistic features (R = 0.66, P < 0.01). All patients with persistent epilepsy (n = 5) had had a treatment lag of over 2 months. Conversely, for all children treated within 2 months (n = 8) spasms ceased within 3 months of treatment and none of them had later epilepsy. This group of patients with a treatment lag of less than 2 months had earlier treatment response (P = 0.002), higher DQ (P = 0.004) and lower score of autistic features (P = 0.006). The data stress the importance of a short treatment lag in view of mental development and prevention of later epilepsy and autistic features, and raise the question of antiepileptogenic effect in this specific condition. (C) 2003 Elsevier B.V. All rights reserved
Starting and stopping treatment.
No full textEpilepsy develops in about 1% of people. The decision to start antiepileptic drug treatment is a diffucult one. It must be based on the risk-benefit ratio; subsequently, questions must be addressed regarding with which drug to use, and for how long. Finally, criteria for terminating treatment must be explained to the patient from the onset of treatmen
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
AEDS EFFICACY IN THE DRAVET SYNDROME: A CROSS-SECTIONAL STUDY
No full textPurpose: Dravet syndrome (DS) is a rare epilepsy with seizures’ onset
during the first year of life. SCN1A gene abnormalities are detected in
about 80% of patients. We aimed to evaluate the efficacy of AEDs in a
large series of this pharmacoresistant epilepsy.
Method: This is a cross-sectional study on all our patients with DS and
SCN1A mutations who had a visit within 2010–2013. We included 54
patients (32 M and 22 F), aged from 2 to 23 years. We reviewed the
characteristics of seizures (age of onset, type, duration, frequency and
day/night prevalence) in relation to the AEDs used and patient0
s age.
Results: Only 5 patients (9%) were seizure free for more than 1 year.
Seizures were mainly fever sensitive. In the oldest patients (>10y) compared
to youngers (6–10 years), seizures were most often tonic-clonic
(86% vs. 36% in each group respectively), shorter (<1 min in 55% vs. 1–
5 min in 64%), sleep-related (55% vs. 36%), and rather more frequent
(weekly in 55% vs. monthly in 71%).
Fourty patients (74%) received a tritherapy (VPA, STP, CLB), associated
with another AED in 30 (74%) of them (TPM, LEV, ZNG, CZP, ketogenic
diet, bromide, canabidiol).
Convulsive status epilepticus (SE) disappeared in 48% of patients
after the introduction of STP. However, 5 children (9%) still experienced
SE after 6 years and one after 11 years, mainly in the context of fever.
Conclusion: Despite the decrease of status epileptics and long lasting
seizures with tritherapy (STP, VPA, CLB), <10% of patients are seizure
free and half remain with weekly seizures up to adulthood. These preliminary
data suggest that there is still a need for developing and evaluating
new AEDs in DS
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