Piracetam and Seizures
Allegations of increased seizure risk from piracetam have been made by a few US physicians associated with establishment DS organizations. This is of special concern due to a higher-than-normal incidence of seizures in DS individuals. The basis of these allegations of seizure risk is enhanced cellular calcium influx from piracetam, an in vitro (test-tube) finding whose applicability to real life must be seriously questioned in the face of decades of clinical experience to the contrary [see SDN v5n8p10]. In fact, piracetam has mild anti-seizure activity, and it protects against memory and cognitive deficits caused by seizures.
Piracetam is used as an adjunctive therapy for epilepsy. Although its effects on epilepsy are not considered sufficiently substantive when used alone, piracetam does potentiate the antiepileptic activity of other drugs. Some newer “racetam” analog drugs appear to have stronger anticonvulsant activity.
Piracetam is recognized throughout most of the world as a treatment of choice for myoclonus, a seizure-like condition characterized by uncontrolled muscle twitching or jerking. This application of piracetam has been thoroughly researched from a clinical perspective. Piracetam has orphan drug status in the US for treatment of myoclonus.
In a recent study of 60 patients, piracetam was found to be “effective in myoclonus, especially that of cortical origin” when used either singly and with other drugs [Ikeda et al., 1996]. Although this study was open-label, a blinded video inspection was employed. Piracetam was of positive benefit to handwriting, feeding, sleep, attention deficit, depression, gait ataxia (incoordination), and convulsions, but not to dysarthria (articulation difficulty). This latter finding is somewhat paradoxical, given that enhancement of speech and language skills is generally the rule rather than the exception. There was also “no positive correlation between clinical and electrophysiological [EEG] improvement,” suggesting that piracetam works through a different mechanism than standard anticonvulsant drugs.
In an earlier study, myoclonic patients with positive clinical responses to piracetam (2.4 to 16.8 g/day) were studied in a placebo-controlled, double-blind, two-week, cross-over trial. Of 21 patients with “disabling spontaneous, reflex or action myoclonus due to various causes,” 10 had to be rescued from the placebo phase of the study due to severe exacerbations of their myoclonus [Brown et al., 1993]. No patients required rescuing from the piracetam arm. Piracetam improved motor function scores, writing ability, functional disability scores, global assessment scores, and visual tests. The authors concluded, “Piracetam, usually in combination with other antimyoclonic drugs, is a useful treatment for myoclonus of cortical origin.”
The dose of piracetam may be quite large in some circumstances and still be well tolerated. In one case of accidental electrocution, spastic tetraparesis (limb paralysis) and spontaneous myoclonus (muscle twitching) in both arms were successfully controlled by 24 g/day piracetam, administered intravenously [Karacostas et al., 1993]. The myoclonic movements returned three days after the piracetam was discontinued six weeks into therapy, and were almost abolished when the piracetam was resumed.
A review of the treatment of myoclonus with piracetam covering “62 case reports, 3 open trials and 2 double-blind trials, covering 171 patients” has been published [Van Vleymen and Van Zandijcke, 1996]. A clinical review of the symptoms and diagnosis of myoclonus, progressive myoclonus epilepsy and other epilepsies, and the use of piracetam and 5-hydroxytryptophan in recent clinical trials, has also been published in Nurse Practitioner [Tate, 1995].
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