Seizures induced by movement: report of a case relieved by operation

Falconer, Murray A.; Driver, M. V.; Serafetinides, E. A.

doi:10.1136/jnnp.26.4.300

Cited by 56 publications

(15 citation statements)

References 6 publications

(7 reference statements)

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“…The observations that most EEGs show no seizure activity, that attacks do not evolve into generalised or focal convulsions, and that there are no alterations in consciousness support a subcortical focus [20]. Falconer and colleagues [8] described a patient with "seizures induced by movement" in whom excision of a cortical scar from the left supplementary motor cortex resulted in cessation of attacks. However, closer inspection of the case shows many features atypical of PKC and suggests that his case was probably frontal lobe epilepsy.…”

Section: Discussionmentioning

confidence: 99%

Paroxysmal kinesigenic choreoathetosis: a report of 26 patients

Bhatia

et al. 1999

Journal of Neurology

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Paroxysmal kinesigenic choreoathetosis (PKC) is a neurological condition which results in abnormal involuntary movements that are precipitated by sudden movement. Because of its rarity, large case series of PKC have not been published. We studied 26 patients with PKC, which represents the largest series thus reported. We reviewed our cases with respect to attack characteristics, aetiology, family history, and treatment response. Our population consisted of 23 men and 3 women. Seven patients had a family history of paroxysmal dyskinesia. None of our patients had clear evidence of symptomatic PKC. Two-thirds of our patients had attacks lasting between 30-60 s, and over one-half experienced one to ten attacks per day. Attack distribution varied widely, and most experienced pure dystonia rather than choreodystonic movements. Most patients responded very well to anticonvulsant therapy. We also report the PET results from two of our patients and Bereitschaftspotential abnormalities recorded from two others.

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Section: Discussionmentioning

confidence: 99%

Paroxysmal kinesigenic choreoathetosis: a report of 26 patients

Bhatia

et al. 1999

Journal of Neurology

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“…Many authors regard PKC as a form of reflex epilepsy involving the thalamus or the basal ganglia [19][20][21]. Many authors regard PKC as a form of reflex epilepsy involving the thalamus or the basal ganglia [19][20][21].…”

Section: Pathophysiology Of Pkcmentioning

confidence: 99%

“…Their main arguments are the paroxysmal nature of the attacks, the non-progressive and remitting character of the disorder and the excellent response to anticonvulsants [20]. In support of the epilepsy theory is the patient described by Falconer et al [21]. In support of the epilepsy theory is the patient described by Falconer et al [21].…”

Section: Pathophysiology Of Pkcmentioning

confidence: 99%

“…The arguments in favour of a subcortical focus and not a cortical one are the absence of seizure discharges on electroencephalogram (EEG) in the majority of cases, the absence of evolution of the attacks into generalized or focal convulsions and the lack of an associated loss of consciousness or amnesia [20]. In this patient who had "seizures induced by movement", an excision of a cortical scar from the left supplementary motor cortex resulted in cessation of attacks [21]. In this patient who had "seizures induced by movement", an excision of a cortical scar from the left supplementary motor cortex resulted in cessation of attacks [21].…”

Section: Pathophysiology Of Pkcmentioning

confidence: 99%

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The paroxysmal dyskinesias

Bhatia

1999

Journal of Neurology

111

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The clinical, pathophysiological and genetic features of some of the paroxysmal movement disorders are reviewed. Paroxysmal kinesigenic choreoathetosis/dyskinesias (PKC/PKD) is a condition in which brief and frequent dyskinetic attacks are provoked by sudden movement. PKC is more common in men and can be idiopathic (commonly familial) or due to a variety of causes. The pathophysiology of PKC is uncertain but it could be an ion-channel disorder. Antiepileptic drugs particularly carbamazepine are very helpful in a large proportion of cases. Paroxysmal exercise induced dystonia (PED) is a rare disorder manifesting as episodes of dystonia mostly affecting the feet induced by continuous exercise like walking or running. Although the initial cases were familial, there is a higher proportion of sporadic cases. The pathophysiology of PED is unknown and antiepileptic drugs are generally unhelpful. In paroxysmal dystonic choreoathetosis/non-kinesigenic dyskinesias (PDC/PNKD) the attacks are of long duration and induced by variety of factors including coffee, tea, alcohol and fatigue but not by sudden movement. PDC can be idiopathic (familial or sporadic) or symptomatic due to a variety of causes. The gene for familial PDC has been linked in 2 families to chromosome 2 q close to a cluster of ion channel genes again suggesting that this disorder may also be a channelopathy. Other paroxysmal disorders include paroxysmal nocturnal dyskinesia, a form of frontal lobe epilepsy in some cases which may be familial with autosomal dominant inheritance (ADNFLE). The gene for ADNFLE in one family has been found to be a mutation in the neuronal acetylcholine receptor gene (CHRNA4) on chromosome 20q. Tonic spasms in multiple sclerosis and Sandiffers syndrome producing intermittent torticollis in infants and children are other paroxysmal movement disorders.

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“…The frequency may be as high as 100 attacks each day. A subgroup can also be recognized of dystonic seizures caused by an identifiable lesion of the brain, for example, cerebral palsy [23], a cortical scar [3], multiple sclerosis [ 161, or basal ganglia disease [33]. …”

mentioning

confidence: 99%

Familial paroxysmal dystonic choreoathetosis and its differentiation from related syndromes

Lance

1977

Annals of Neurology

288

143

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Four generations of a family are described in which 7 of 8 affected members suffered from prolonged dystonic seizures; the eighth member's attacks were those of paroxysmal choreoathetosis. The attacks lasted up to 4 hours, were precipitated by alcohol, emotion, or fatigue, and responded poorly to phenytoin and barbiturates but were controlled by clonazepam. Autopsy on an affected child who died a "crib death" at the age of 2 years disclosed no major abnormality of the brain. This family appears to have the same condition as that described by Mount and Reback in 1940, Forssman in 1961, and Richards and Barnett in 1968, which the last authors termed paroxysmal dystonic choreoathetosis to distinguish it from the more common movement-induced (kinesigenic) form of the disorder. Analysis of reports of 100 cases of paroxysmal kinesigenic choreoathetosis shows that the attacks last less than 5 minutes, are precipitated by sudden movement or startle, and usually respond well to phenytoin or barbiturates. A clinical classification is presented in which the kinesigenic form is divided into a familial group (72% of cases) and a sporadic group (28% of cases) and contrasted with paroxysmal dystonic choreoathetosis. One family with an intermediate form, in which dystonic choreoathetosis was provoked by continued exertion and lasted for up to 30 minutes, is also reported.

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Seizures induced by movement: report of a case relieved by operation

Cited by 56 publications

References 6 publications

Paroxysmal kinesigenic choreoathetosis: a report of 26 patients

Paroxysmal kinesigenic choreoathetosis: a report of 26 patients

The paroxysmal dyskinesias

Familial paroxysmal dystonic choreoathetosis and its differentiation from related syndromes

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