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Functional Sequelae (functional + sequelae)

Distribution by Scientific Domains

Medical Sciences	80%

Selected Abstracts

Outcome after prolonged convulsive seizures in 186 children: low morbidity, no mortality

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 1 2004
Piia Metsäranta BM
Prolonged convulsive seizures are a common neurological emergency and a potential cause of neuronal damage and functional sequelae. We explored the role of seizure duration and various background factors for neurological sequelae in children with prolonged convulsive seizures. The population-base of this study was all children (age < 16 years) who had been admitted to the Tampere University Hospital, Finland between 1993 and 1999 with convulsive seizures lasting more than 5 minutes. Patients were followed up individually (mean length of follow-up 2 years 1 month, range 0 to 7 years 8 months). All available data on the prolonged seizure episodes and clinical follow-up were analyzed retrospectively by a detailed review of all medical charts and records. In 186 children (94 males, 92 females; mean age 4 years 5 months, SD 3 years 10 months, range 1 month to 15 years 4 months) there were 279 separate convulsive seizure episodes lasting over 5 minutes, yielding an annual incidence of 47.5 out of every 100000 episodes. Seizure aetiology was idiopathic in 26.2% of episodes, febrile in 41.9%, remote symptomatic in 28%, and acute symptomatic in 3.9% of episodes. Mean duration of all seizure episodes was 42.5 minutes (SD 46.1 minutes) and was significantly correlated with the aetiology: shortest in the febrile group (mean 35.4 minutes) and longest in the acute symptomatic group (mean 88.6 minutes; p < 0.001). There was no mortality related directly to these acute seizure episodes. The most common sequela was an onset of epilepsy in 40 children (22%). Permanent neurological sequelae were noted in only four patients (2.2%; mean seizure duration 16 minutes) and non-permanent sequelae in six patients (3.2%; mean seizure duration 38 minutes). Neurological sequelae of prolonged convulsive seizures in children are rare and are related to aetiological factors rather than the duration of a single seizure. The role of acute seizures in the evolution of epilepsy in children remains obscure. [source]

Neurotoxicity of methylenedioxyamphetamines (MDMA; ecstasy) in humans: how strong is the evidence for persistent brain damage?

ADDICTION, Issue 3 2006
E. Gouzoulis-Mayfrank
ABSTRACT Background The popular dance drug ecstasy (3,4-methylenedioxymethamphetamine: MDMA and some analogues) causes selective and persistent neurotoxic damage of central serotonergic neurones in laboratory animals. Serotonin plays a role in numerous functional systems in the central nervous system (CNS). Consequently, various abnormalities including psychiatric, vegetative, neuroendocrine and cognitive disorders could be expected in humans following MDMA-induced neurotoxic brain damage. Aims In recent years, the question of ecstasy-induced neurotoxicity and possible functional sequelae has been addressed in several studies with drug users. The aim of this paper was to review this literature and weigh the strength of the evidence for persistent brain damage in ecstasy users. Methods We used Medline to view all available publications on ,ecstasy' or ,MDMA'. All available studies dealing with ecstasy users entered this analysis. Findings and conclusions Despite large methodological problems the bulk of evidence suggests residual alterations of serotonergic transmission in MDMA users, although at least partial restitution may occur after long-term abstinence. However, functional sequelae may persist even after longer periods of abstinence. To date, the most consistent findings associate subtle cognitive, particularly memory, impairments with heavy ecstasy use. However, the evidence cannot be considered definite and the issues of possible pre-existing traits or the effects of polydrug use are not resolved. Recommendations Questions about the neurotoxic effects of ecstasy on the brain remain highly topical in light of its popularity among young people. More longitudinal and prospective studies are clearly needed in order to obtain a better understanding of the possible long-term sequelae of ecstasy use in humans. [source]

Physical sequelae and self-perceived attachment in adult survivors of childhood cancer

PSYCHO-ONCOLOGY, Issue 4 2001
David Joubert
The association between the physical sequelae of childhood cancer and self-reported attachment behavior was investigated in 97 adult survivors. Attachment was assessed using standardized self-report questionnaires. Functional disability and cosmetic sequelae of the cancer and its treatment were evaluated by the attending oncologist using a standardized rating scale. Results suggest that attachment is not significantly associated with physician-rated physical sequelae, but may be related to the time of onset of the functional deficits, independent of the current age or age at diagnosis. Further, survivors with functional sequelae in adulthood describe themselves as more insecure in their relationships in general and more ambivalent in their relationship with their parents. These findings, if replicated, suggest that the duration of the functional deficits as well as the developmental stage of the individual when they began may be important variables which affect the survivor's capacity to develop and maintain intimate relationships that are secure and satisfying. Copyright © 2001 John Wiley & Sons, Ltd. [source]

The familial hypertrophic cardiomyopathy-associated myosin mutation R403Q accelerates tension generation and relaxation of human cardiac myofibrils

THE JOURNAL OF PHYSIOLOGY, Issue 15 2008
Alexandra Belus
The R403Q mutation in ,-myosin heavy chain was the first mutation to be identified as responsible for familial hypertrophic cardiomyopathy (FHC). In spite of extensive work on the functional sequelae of this mutation, the mechanism by which the mutant protein causes the disease has not been definitely identified. Here we directly compare contraction and relaxation mechanics of single myofibrils from left ventricular samples of one patient carrying the R403Q mutation to those from a healthy control heart. Tension generation and relaxation following sudden increase and decrease in [Ca2+] were much faster in the R403Q myofibrils with relaxation rates being the most affected parameters. The results show that the R403Q mutation leads to an apparent gain of protein function but a greater energetic cost of tension generation. Increased energy cost of tension generation may be central to the FHC disease process, help explain some unresolved clinical observations, and carry significant therapeutic implications. [source]