Book contents
- Frontmatter
- Contents
- List of contributors
- Preface and overview
- 1 Epilepsies as channelopathies
- 2 Epilepsy and movement disorders in the GABAA receptor β3 subunit knockout mouse: model of Angelman syndrome
- 3 Genetic reflex epilepsy from chicken to man: relations between genetic reflex epilepsy and movement disorders
- 4 Functional MRI of the motor cortex
- 5 Neuromagnetic methods and transcranial magnetic stimulation for testing sensorimotor cortex excitability
- 6 Motor dysfunction resulting from epileptic activity involving the sensorimotor cortex
- 7 Nocturnal frontal lobe epilepsy
- 8 Motor cortex hyperexcitability in dystonia
- 9 The paroxysmal dyskinesias
- 10 Normal startle and startle-induced epileptic seizures
- 11 Hyperekplexia: genetics and culture-bound stimulus-induced disorders
- 12 Myoclonus and epilepsy
- 13 The spectrum of epilepsy and movement disorders in EPC
- 14 Seizures, myoclonus and cerebellar dysfunction in progressive myoclonus epilepsies
- 15 Opercular epilepsies with oromotor dysfunction
- 16 Facial seizures associated with brainstem and cerebellar lesions
- 17 Neonatal movement disorders: epileptic or non-epileptic
- 18 Epileptic and non-epileptic periodic motor phenomena in children with encephalopathy
- 19 Epileptic stereotypies in children
- 20 Non-epileptic paroxysmal eye movements
- 21 Shuddering and benign myoclonus of early infancy
- 22 Epilepsy and cerebral palsy
- 23 Sydenham chorea
- 24 Alternating hemiplegia of childhood
- 25 Motor attacks in Sturge–Weber syndrome
- 26 Syndromes with epilepsy and paroxysmal dyskinesia
- 27 Epilepsy genes: the search grows longer
- 28 Genetics of the overlap between epilepsy and movement disorders
- 29 Seizures and movement disorders precipitated by drugs
- 30 Steroid responsive motor disorders associated with epilepsy
- 31 Drugs for epilepsy and movement disorders
- Index
- Plate section
29 - Seizures and movement disorders precipitated by drugs
Published online by Cambridge University Press: 03 May 2010
- Frontmatter
- Contents
- List of contributors
- Preface and overview
- 1 Epilepsies as channelopathies
- 2 Epilepsy and movement disorders in the GABAA receptor β3 subunit knockout mouse: model of Angelman syndrome
- 3 Genetic reflex epilepsy from chicken to man: relations between genetic reflex epilepsy and movement disorders
- 4 Functional MRI of the motor cortex
- 5 Neuromagnetic methods and transcranial magnetic stimulation for testing sensorimotor cortex excitability
- 6 Motor dysfunction resulting from epileptic activity involving the sensorimotor cortex
- 7 Nocturnal frontal lobe epilepsy
- 8 Motor cortex hyperexcitability in dystonia
- 9 The paroxysmal dyskinesias
- 10 Normal startle and startle-induced epileptic seizures
- 11 Hyperekplexia: genetics and culture-bound stimulus-induced disorders
- 12 Myoclonus and epilepsy
- 13 The spectrum of epilepsy and movement disorders in EPC
- 14 Seizures, myoclonus and cerebellar dysfunction in progressive myoclonus epilepsies
- 15 Opercular epilepsies with oromotor dysfunction
- 16 Facial seizures associated with brainstem and cerebellar lesions
- 17 Neonatal movement disorders: epileptic or non-epileptic
- 18 Epileptic and non-epileptic periodic motor phenomena in children with encephalopathy
- 19 Epileptic stereotypies in children
- 20 Non-epileptic paroxysmal eye movements
- 21 Shuddering and benign myoclonus of early infancy
- 22 Epilepsy and cerebral palsy
- 23 Sydenham chorea
- 24 Alternating hemiplegia of childhood
- 25 Motor attacks in Sturge–Weber syndrome
- 26 Syndromes with epilepsy and paroxysmal dyskinesia
- 27 Epilepsy genes: the search grows longer
- 28 Genetics of the overlap between epilepsy and movement disorders
- 29 Seizures and movement disorders precipitated by drugs
- 30 Steroid responsive motor disorders associated with epilepsy
- 31 Drugs for epilepsy and movement disorders
- Index
- Plate section
Summary
Antiepileptic drugs as a cause of worsening of seizures
The paradoxical ability of antiepileptic drugs (AED) to induce worsening of seizures has been identified from the very beginning of AED treatment (Zaccara et al., 1990, Garcia & Alldredge, 1994, Stimmel & Dopheide, 1996). It is often overlooked by the non-specialist, who is therefore reluctant to remove the causative agent, even when the patient or relatives have identified the relationship. When children are involved at the onset of their epilepsy, this phenomenon could adversely affect the long-term prognosis. There is accumulating evidence that, in certain epilepsies, such as West syndrome, prevention of seizure recurrence from the very beginning may also prevent the development of cognitive troubles and epilepsy as a chronic disorder. Identification of prognostic factors and a greater awareness of this concept, especially at the primary care level, is therefore most important.
Deterioration in seizure frequency after administration of antiepileptic drugs can occur (i) as a non-specific manifestation of overdose or (ii) as a relatively specific effect on selected seizure types.
Intoxication as a cause of seizure worsening
It has been recognized for many years and seems to be more common than generally thought. Among patients admitted to the Chalfont Centre for Epilepsy in the early 1970s with a clinical diagnosis of antiepileptic drug intoxication, 25% were reported to exhibit paradoxical seizure worsening (Laidlaw et al., 1980).
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- Epilepsy and Movement Disorders , pp. 465 - 510Publisher: Cambridge University PressPrint publication year: 2001