Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A combined informant questionnaire and interview survey of self-injurious behavior (SIB) at a large state facility for the retarded was conducted independently three times over a 3-year period. Prevalence consistently was about 10% of the population. SIB cases tended to be younger and institutionalized longer than the rest of the population. Severe cases had a longer history of chronic SIB. SIB cases had more seizure disorders, severe language handicaps, visual impairments, and severe or profound retardation than the rest of the population. They appeared to fulfill most of the Rutter (1966) criteria for autism. But unlike the severely autistic, there was little relation of sex to incidence of SIB. Over 90% of SIB cases changed status over 3 years, suggesting that SIB was amenable to behavior modification in most cases (94%). Psychotropic behavior control medications helped in some intervention programs (32%). SIB remitted spontaneously in 21% of SIB cases where there had been no behavioral or drug intervention.
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PMID:Prevalence of self-injurious behaviors in a large state facility for the retarded: a three-year follow-up study. 2 30

Administration of the selective D1-dopamine receptor agonist 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine (SKF-38393) to neonatal 6-hydroxydopamine-lesioned rats results in profound behavioral manifestations and induction of striatal c-fos-like immunoreactivity. The full D1-dopamine agonist I,[R,S]1-aminomethyl-3,4-dihydro-5,6-dihydroxy-3-phenyl-1H-2-benzopyran hydrochloride (A-68930), like SKF-38393, produced a dose-dependent, D1-selective increase in locomotor activity and striatal c-fos-like immunoreactivity. These responses were antagonized by a D1-dopamine antagonist, but not by a D2-dopamine antagonist. A-68930 produced locomotor activation at a lower dose than SKF-38393, but no dose of A-68930 was able to produce the magnitude of locomotor activation seen with SKF-38393. Both A-68930 and SKF-38393 induced similar stereotyped behaviors and possessed similar propensities to induce self-injurious behavior in neonatally lesioned rats; however, A-68930 was significantly more potent than SKF-38393 in inducing these behaviors. When either SKF-38393 or A-68930 were administered repeatedly at 2-week intervals, behavioral sensitization (priming) occurred. However, unlike SKF-38393, a high dose of A-68930 produced seizure activity and markedly desensitized D1-dopamine receptor activation for up to 3 days after administration. These results with A-68930 provide additional evidence that the specific behavioral and biochemical responses observed in neonatally lesioned rats after SKF-38393 administration are due to actions on D1-dopamine receptors, and indicate that A-68930 provides a new tool for investigating D1-dopamine receptor function.
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PMID:Comparison of the D1-dopamine agonists SKF-38393 and A-68930 in neonatal 6-hydroxydopamine-lesioned rats: behavioral effects and induction of c-fos-like immunoreactivity. 135 57

An adult female with developmental disability was prescribed chlorpromazine for the target behaviors of aggression and self-injurious behavior (SIB), and she was prescribed phenobarbital for seizures. Upon a chlorpromazine minimal effective dose reduction, target behaviors increased and dosage was returned to prior levels with the conclusion that chlorpromazine was controlling the target behaviors. Upon subsequent reduction and discontinuation of phenobarbital, however, chlorpromazine was able to be reduced with no increase in target behaviors. Ten years of behavioral data are presented to support the hypothesis that phenobarbital was exacerbating maladaptive behaviors. Given tardive dyskinesia (TD), clinicians and interdisciplinary teams should remain alert to the following client profile: (1) prescribed phenobarbital (or primidone), (2) prescribed neuroleptics, especially at high dosages, to control maladaptive behaviors, (3) failure of neuroleptic gradual minimal effective dose attempts, and (4) possible presence of behavioral procedures, especially intrusive procedures, to control maladaptive behaviors. This profile should trigger a "red flag" as to the possibility of phenobarbital behavioral side effects or exacerbation of preexisting maladaptive behaviors.
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PMID:A case of phenobarbital exacerbation of a preexisting maladaptive behavior partially suppressed by chlorpromazine and misinterpreted as chlorpromazine efficacy. 150 79

The contemporary behavior analyst, to operate ethically and effectively, must be aware of many more factors affecting behavior than simple consequences. Although the literature demonstrating the effectiveness of active behavior management is impressive, a compelling argument can be made that a great number of behavior problem seen in individuals with developmental disabilities may be attributable to factors other than consequences. Our experience has been more often than not that physiological, organic, medication, or situational variables are the actual culprits in maladaptive behavior. Individuals with severe or profound retardation may respond to aversive features of their environment by displaying noncompliance, tantrums, aggression, or self-injurious behavior. These antecedents can affect their behavior just as powerfully as can the consequences of their behavior. Behavior analysts must become sensitive to these potential factors and be prepared to employ behavioral diagnostic strategies in the search for the causes of maladaptive behavior. Finally, they must be prepared to design rather unconventional passive behavior management treatment programs involving the manipulation of the antecedent environment. In the case of Carrie, from the example at the beginning of this paper, the analysis yielded the hypothesis that her face scratching was a reaction to sinus blockage caused by seasonal allergies. Her treatment involved daily dosages of antihistamines administered by our nurses and subsequent elimination of the scratching. Tom was found to be suffering from "wheelchair fatigue." When he was allowed to recline on other surfaces (e.g., bean bag chair, mat, bolster) on a regular basis, he did not attempt any form of self-injury. Melissa was found to have a severe case of Pre Menstrual Syndrome as well as seizure disorder, and was treated with the appropriate medications. Her headbanging was reduced to a few minor incidents per month. Walter's tantrums on closer inspection seemed part of a chain of behavior leading to seizure-like attacks. Preliminary evidence suggests that when he is treated with phenobarbital the tantrums and aggression disappear. And finally, Debbie was found to be very sensitive to a variety of discomforting events. She would cry, sob, and scream when she was wet, thirsty, hungry, and tired. Changing her regularly, offering her water every hour and extra snacks in the morning as well as short naps in the early afternoon eliminated the crying and sobbing. She now participates with the other clients and seems to enjoy the house activities.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Behavioral diagnostics. 274 44

We report the results of an open trial of valproic acid in the treatment of affective symptoms in people with mental retardation. The study population consisted of 209 people with mental retardation who were serially referred to a tertiary-care medical center for the evaluation of behavioral symptoms. Criteria for treatment included the presence of three of the four following symptoms: irritability, sleep disturbance, aggressive or self-injurious behavior, and behavioral cycling. Twenty-one patients met enrollment criteria and were studied prospectively for a 2-year period. Two patients were lost to follow-up. One patient experienced severe drug side effects. Eighteen patients completed the study. Fourteen patients (78%) responded favorably to treatment and were maintained on valproic acid for the 2 years of the study (p < 0.001). Medications prescribed at the time of enrollment were usually discontinued, including neuroleptic medication in 9 of 10 patients and in all patients (N = 3) who were receiving phenobarbital. A history of epilepsy or a suspicion of seizures was strongly associated with a favorable response to valproic acid (p < 0.005). The results of this study suggest that people with mental retardation and concurrent affective disorders can be recognized by a cluster of developmentally appropriate symptoms such as those listed above. In addition, affective symptoms can be successfully treated with valproate with reductions in neuroleptic and barbiturate anticonvulsant medication. Further study of the comparative benefit of valproate and carbamazepine in this population is warranted.
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PMID:Long-term administration of valproic acid in the treatment of affective symptoms in people with mental retardation. 812 Jan 59

Measurement methods from behavioral psychology were used to assess antiepileptic drug behavioral side effects in 5 individuals with mental retardation. When the suspected antiepileptic drug was altered, an 81% reduction of maladaptive behaviors occurred. Quality of life outcomes included successful community placement and termination of an aversive intervention procedure. Three cases demonstrated antiepileptic drug exacerbation of disruptive vocalizations, agitation, self-injurious behavior, and property destruction; 2 demonstrated improved aggression, but illustrated a common clinical problem. When seizure control must be maintained and a suspected antiepileptic drug cannot be reduced before a second antiepileptic drug with potential psychotropic properties is initiated, it was not possible to absolutely conclude that the first antiepileptic drug was responsible for the behavior problem. Overall, these measurement methods were instrumental in the systematic clinical evaluation of antiepileptic drug behavioral side effects in individuals unable to verbally communicate the presence of these side effects.
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PMID:Antiepileptic drug behavioral side effects in individuals with mental retardation and the use of behavioral measurement techniques. 856 87

The efficacy of the serotonin (5-HT) uptake inhibitor clomipramine in the treatment of self-injurious behavior (SIB) was tested in individuals with severe and profound mental retardation. Six of the 8 subjects who completed a double-blind, placebo-controlled crossover trial exhibited a clinically significant improvement (50% or greater reduction from placebo) in the frequency of SIB. Clomipramine treatment was also associated with improvement in SIB intensity, frequency of stereotypy and compulsions, teacher ratings of stereotypy and social withdrawal, and frequency of staff intervention required for problem behaviors. Adverse effects (seizure and tachycardia/agitation) occurred in 2 of the 8 subjects. These results represent the first controlled trial of a 5-HT uptake inhibitor in the treatment of SIB in mental retardation.
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PMID:Clomipramine treatment for self-injurious behavior of individuals with mental retardation: a double-blind comparison with placebo. 873 78

The goal of epilepsy monitoring is to capture several seizures, utilizing continuous electroencephalography (EEG)/video for later analysis. Various provocative techniques, such as withdrawing antiepileptic drugs or sleep deprivation are used to precipitate seizures. Patients run a higher risk of injuries due to having an increase in seizure frequency and/or intensity or a change in seizure type. Evaluating the potential for, and preventing injuries is an important part of risk management. However, very little information has been published regarding safety issues in an epilepsy monitoring unit (EMU). Several types of safety issues have been identified during monitoring: uncontrolled behavior (ictal and post-ictal aggression, self injurious behavior, psychosis); seizure related injuries (falls, status epilepticus); problems related to electrodes (pulling out scalp and surgically implanted electrodes); and specific concerns regarding children in the EMU. Use of restraints and sitters in selected patients, appropriate medication for psychosis, shock absorbing carpet and "child-proofing" rooms for the young are among the preventative actions discussed. Central to risk management is the education of the staff in the assessment of each patient's potential for injury and use the appropriate interventions. Consideration should be given to balancing the need to avert harm, with an unrestricted environment.
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PMID:Safety in long-term EEG/video monitoring. 895 Jun 95

This single case reports an open trial of lamotrigine in the treatment of self-injurious behavior (SIB) and epilepsy in an 18-year-old female diagnosed with generalized seizure disorder, stereotypic movement disorder, and compulsive SIB in the context of profound mental retardation. Animal models of SIB suggest that the glutamate neurotransmitter systems, involved in the generation of epileptic seizures, may also have a role in the pathophysiology of SIB. Data suggesting that lamotrigine may decrease glutamate release encouraged an empirical trial of lamotrigine for treatment of SIB. After 4 weeks of treatment of lamotrigine 200 mg daily, decreases in agitation and fearfulness were clinically observed, along with a 50% reduction in the frequency of SIB as measured by standardized scales. Good seizure control was maintained throughout the trial. No significant adverse effects were observed. Positive effects persisted at 1-year follow-up. Symptoms of stereotypic movement disorder appeared unchanged. Because these findings are preliminary, no clinical recommendations for the treatment of SIB with lamotrigine can be made until controlled studies have been completed.
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PMID:Open trial lamotrigine in the treatment of self-injurious behavior in an adolescent with profound mental retardation. 923 20

We report a family with a heterogeneous group of neurologic disorders associated with the mitochondrial DNA G8363A transfer ribonucleic acid (RNA)Lys mutation. The phenotype of one child in the family was consistent with autism. During his second year of life, he lost previously acquired language skills and developed marked hyperactivity with toe-walking, abnormal reciprocal social interaction, stereotyped mannerisms, restricted interests, self-injurious behavior, and seizures. Brain magnetic resonance imaging (MRI) and repeated serum lactate studies were normal. His older sister developed signs of Leigh syndrome with progressive ataxia, myoclonus, seizures, and cognitive regression. Her laboratory studies revealed increased MRI T2-weighted signal in the putamen and posterior medulla, elevated lactate in serum and cerebrospinal fluid, and absence of cytochrome c oxidase staining in muscle histochemistry. Molecular analysis in her revealed the G8363A mutation of the mitochondrial transfer RNA(Lys) gene in blood (82% mutant mitochondrial DNA) and muscle (86%). The proportions of mutant mitochondrial DNA from her brother with autism were lower (blood 60%, muscle 61%). It is likely that the origin of his autism phenotype is the pathogenic G8363A mitochondrial DNA mutation. This observation suggests that certain mitochondrial point mutations could be the basis for autism in some individuals.
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PMID:Autism associated with the mitochondrial DNA G8363A transfer RNA(Lys) mutation. 1086 77


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