On the rare occasions that the child is febrile, treatment of possible fever and the underlying illness is also important. This is a genuine paediatric emergency that demands appropriate and vigorous treatment as for status epilepticus. The treatment of prolonged febrile seizures and febrile status epilepticus is described on pages Continuous anticonvulsant treatment is usually not recommended.
Although there are effective therapies that could prevent the occurrence of additional seizures, the potential adverse effects of such therapy are not commensurate with the benefit. The great majority of children with benign focal seizures do not need anticonvulsant treatment even if they suffer lengthy seizures or have more than two recurrences.
The risks are small and the potential side effects of drugs appear to outweigh the benefits. There is no convincing evidence, however, that any therapy will alleviate the possibility of recurrences. In deciding management for a child with benign childhood focal seizures the following should be considered:. Continuous prophylaxis consists of daily monotherapy using any antiepileptic drug with proven efficacy in focal seizures, usually carbamazepine.
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However, carbamazepine may exaggerate seizures in a minority of children with RS. Recently, sulthiame has been revived as an excellent drug for the treatment of benign childhood epilepsy with centrotemporal spikes. Methods of withdrawing medication differ between experts, though all agree that there is no need to continue medication 1—3 years after the last seizure and certainly not after 14 years of age when most benign childhood focal seizures remit or 16 years of age when they are practically non-existent.
My practice is to start gradual withdrawal of medication 2 years after the last seizure, making sure that the child does not have any minor seizures. However, I do not adhere to fixed rules and may continue medication until the age of 13—15 years depending on the severity, frequency and age at onset of seizures. Thus, in a child that had frequent, severe and difficult to control fits in early childhood, I would not stop medication if the child had a seizure-free period of 2—3 years by the age 7 years.
Conversely, for a child who had three or four nocturnal seizures at age 11 and 12 years, I would certainly slowly discontinue medication after a 2-year seizure-free period.
I advise very slow withdrawal, reducing the dose in monthly steps so that the drug is completely discontinued approximately 6 months later. The reason for this is that I expect that any possible seizure recurrence during the process of very slow drug withdrawal would manifest with mild, brief and simple focal without secondary generalised convulsions. In the case of barbiturates and diazepines, slow withdrawal of medication is mandatory in order to avoid risking a possible withdrawal seizure. The traditional goal of care for children with epilepsies has been optimal seizure control.
This has now been widely broadened to include optimal health-related quality of life outcomes. Thus, it is crucial that parents are given sufficient time and opportunity to discuss their concerns with the specialists, who should provide the following:. The adjustment and other problems experienced by children with a diagnosis of epilepsy and their parents have always been a concern to clinicians and health-care providers.
The only exception to this is in relation to febrile seizures where parental reactions and concerns have been well documented — and properly addressed. In one such study, 52 parents of a child with febrile seizures were interviewed about their immediate and long-term reactions. It is now part of good clinical practice to provide the parents of children with febrile seizures specific information about fever and febrile seizures, and comprehensive instructions about what to do if a seizure happens again.
Talking extensively to parents of children with benign childhood focal seizures I realised that, despite the fact that these seizures are of excellent prognosis, they are a dramatic experience for patients and their parents. Consequently, I have initiated an on-going study aiming to define and analyse the psychosocial effects of benign childhood focal seizures on parents and children.
The questionnaire includes questions on beliefs and attitudes about epilepsy, as well as concerns about the prognosis, necessity of evaluation and information on daily care. I hope that the results of my study will assist the patient and parents, inform the physician and, consequently, help to improve the treatment outcome. The doctor told me that because the seizure was longer than half an hour this may affect the brain and that time will tell. We sleep with our daughter in between us on a large bed, and we keep an eye on her as she enters and exits sleep.
What is a focal seizure?
The majority of parents felt uncertain about what this event was and that they were not given sufficient information or reassurance, and some were told that the child had not had a seizure. Initially, some children were diagnosed as having encephalitis, atypical migraine, fainting, gastroenteritis or motion sickness. These results indicate that there is a need for supportive family management, education and specific instructions about emergency procedures in possible subsequent seizures. Demonstrations of first aid practices for seizures are necessary.
Parents who have watched their child during a fit need specific information and psychological support to overcome anxiety and panic. Anxiety may result in overprotection, which interferes with parent-child separation and independence. Educating parents about the epilepsies and different types of seizure through seminars, courses and lectures will help to alleviate the social stigma surrounding these conditions, which parents often pass on to their children who are the patients. Medicine can now profit from a holistic approach to care through counselling and helping people with epilepsies and their families.
Practice parameter guidelines regarding parental management and education of children with benign seizures should be updated. Benign childhood focal seizures with focal EEG sharp slow wave complexes are a group of syndromes of probably one disease, which, in my opinion, share common clinical and EEG characteristics. Seizures are infrequent, usually nocturnal and remit within 1—3 years from onset. Ictal autonomic manifestations, such as hypersalivation, vomiting, headache, pallor or sweating, and ictal syncope, which is unusual in other epileptic syndromes, are frequent and may occasionally appear in isolation.
The clinical and EEG characteristics of one syndrome may evolve into another or a child may simultaneously develop features of another form of benign childhood focal seizures. Febrile seizures are common. Neurological examination and intellect are normal, but some children may experience mild and reversible neuropsychological problems during the active stage of the disorder. Brain imaging is normal. There are usually severe EEG abnormalities, which are disproportionate to the frequency of seizures.
Epileptogenic foci, irrespective of their location, manifest as abundant, high amplitude, sharp, slow wave complexes that occur mainly in clusters. They are often bilateral, independent or synchronous, frequently combined with foci from other cortical areas or brief generalised discharges, and are exaggerated in sleep stages I—IV.
A unified concept of benign childhood focal seizures is also suggested by the frequency of more than one type of benign childhood focal seizures in an affected child, siblings or both. It is likely and I have proposed that all these conditions are linked together by a common, genetically determined, mild and reversible, functional derangement of the brain cortical maturational process.
The remaining minority have infrequent focal seizures with symptoms that are also localisation- and age-related and -dependent. It is possible that a few of these children, with or without seizures, also have usually minor and fully reversible neuropsychological symptoms that are rarely clinically overt and that can only be detected by formal neuropsychological testing.
My overall impression is that benign childhood focal seizures, their clinical and EEG manifestations and evolutions, need appropriate prospective studies, such as those performed for febrile seizures. One of the most interesting aspects of benign childhood seizures is their striking age-related sequence. Common benign seizure disorders are specific to children and do not occur in adults. The fact that children are particularly susceptible to seizures is well documented.
There are three main periods of age-related childhood susceptibility to seizures. Febrile mainly generalised convulsions first appear in early childhood at a peak age of 18—22 months. Rolandic focal seizures occur in late childhood at a peak age of 7—10 years. Panayiotopoulos syndrome covers the intermediate period, occurring at a peak of 4—5 years, and manifests with mainly autonomic seizures Figure 9.
Let me analyse this further as this is likely to be highly significant in our understanding of the disordered age-related maturational processes. Diagramatic age-related presentation of febrile, Rolandic and Panayiotopoulos syndromes. In the first, early period febrile seizures , the brain is vulnerable to seizures that are triggered by fever and mainly manifest with convulsions that are commonly generalised.
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The second intermediate period Panayiotopoulos syndrome consists of spontaneous seizures that are often prolonged for hours and manifest principally with autonomic and mainly emetic symptoms. The third late period Rolandic syndrome consists of spontaneous focal, motor or sensorimotor seizures. These three periods of clinical seizure susceptibility also have peculiar EEG accompaniments.
The EEG is practically normal in the first period of febrile seizures, shows mainly posterior and multifocal spikes in the intermediate period of Panayiotopoulos syndrome and Rolandic spikes in the late period of the Rolandic syndrome. All these indicate that the brain in early childhood has a low threshold to generalised convulsions provoked by fever with a relatively silent EEG spike capacity. Subsequently, the autonomic system and particularly the emetic centres become vulnerable, the seizure discharges may be self-sustained and the cortex exhibits a diffuse epileptogenicity, which is unequally distributed and mainly affects the posterior regions.
Finally, in the third period of late childhood, brain epileptogenicity shrinks to around the Rolandic regions to produce the distinctive clinical and EEG manifestations of the Rolandic syndrome. These are incontrovertible facts that tell us something very important about the developing brain that we have not yet explored. We should also consider the neonatal and the early infantile periods, because they also have their own peculiarities as indicated by the benign familial and non-familial neonatal seizures that occur around the first few days of life, and the benign infantile focal seizures of the Watanabe-Vigevano syndrome.
This point is exemplified by reports of children with neonatal seizures who later developed Rolandic or PS. Lada et al. This was followed by a brief autonomic seizure of PS with ictal vomiting and deviation of the eyes occurred during sleep at 6 years of age; the EEG showed occipital paroxysms. I have also described a boy who, at 8 weeks old, had three focal seizures of right-sided convulsions involving the face and upper limbs benign infantile non-familial seizures of Watanabe-Vigevano syndrome. Subsequent EEGs were normal and treatment stopped at age 10 months.
He was well until the age of 7 years when he started having RS seizures and later developed epilepsy with continuous spikes and waves during slow wave sleep see Figures 6. The brain MRI was normal case Benign isolated focal seizures of adolescence — constitute an idiopathic, short-lived and transient period of seizure susceptibility during the second decade of life.sdc.ascensiondental.com/casol-chica-liberal-busca.php
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This is a seizure susceptibility of the second decade of life with a peak at 13—15 years of age. There is a According to Loiseau and Louiset a quarter of focal seizures with an onset between 12 and 18 years of age have a benign course i. The disorder may account for between 7. Around cases have been described. There are no epileptic events preceding or following this limited seizure period, which lasts for no more than 36 hours. The physical and mental states of the patients are normal. Benign isolated focal seizures of adolescence are not a recognised syndrome in the new diagnostic scheme.
The commonest ictal clinical manifestations are motor, usually without Jacksonian marching, and somatosensory. Visual, vertiginous and autonomic symptoms are reported in one-fifth of cases. Experiential phenomena, such as those seen in temporal lobe seizures, practically never occur. Laboratory tests and brain imaging are normal. The EEG may show some minor, non-specific, abnormalities without spikes or focal slowing.
In a recent report, 9 of 37 cases had functional spikes, which is incompatible with this syndrome; these patients probably suffered from benign childhood focal seizures as described earlier in this chapter. These patients are difficult to diagnose, as there are no specific features at onset to differentiate them from others with similar clinical manifestations, but of different aetiology, such as symptomatic or cryptogenic focal epilepsies. My practice is to investigate all adolescents with onset of focal seizures with MRI and EEG , which, if normal, would make the diagnosis of benign focal seizures of adolescence more likely.
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