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We read this intriguing case report with great interest. However, it
contained two specific weaknesses which undermined its strength, leaving
it inconclusive. The critical point is not whether caffeine excess might
cause seizures (this is known), or the theoretical pathophysiology
(comprehensively discussed in the article), but whether it was the
definitive cause of seizures in this case.
Firstly, without meas...
Firstly, without measuring the serum caffeine concentration (or at
least its metabolite, theophylline - a widely available assay in acute
hospitals for therapeutic purposes) it is impossible to know how much
credence to place on the role of caffeine in this case.
Secondly, there was no mention of serum sodium, potassium or
creatinine kinase measurements. Sodium and potassium gradients across the
cell membrane exert a major effect on the stability of excitable cells,
especially neurone and skeletal muscle respectively. Potassium
gradients are affected directly by hydrogen ion concentrations.
Hypokalaemia predisposes to tachyarrhythmias, potentially leading to
seizures through secondary cerebral anoxia. There is a complex interplay
between electrolyte disturbances (especially hypokalaemia and acid-base
disturbance), cardiac arrhythmias and seizures - each predisposing to the
others, and in turn being predisposed to by the others. Arguably, the
biochemical data in this case were consistent with recent seizure
activity, irrespective of its precipitant.
In a patient with a previous cerebral infarct and 'vascular
encephalopathy', both significant risk factors for seizure, it is very
difficult to know what part each of the relevant contributory factors
played. The reference cited for seizure incidence post-stroke  looks
at the influence of major co-morbidities (which this patient did not
apparently have) on the outcome, in particular mortality, and without
mentioning seizure per se. That said, the incidence of idiopathic
epilepsy is well known to vary greatly by age and other factors, none of
which was discussed quantitatively for this case.
As the report says, any seizure occurs when the seizure threshold is
lowered sufficiently by the prevailing circumstances. With so many
interdependent co-variates in this case (underlying structural brain
lesion, past history of substance abuse and possible withdrawal, acute
kidney injury, electrolyte and acid-base disturbances, as well as possible
rhabdomyolysis) in addition to the possibility of caffeine, it is
impossible to judge the latter's likely contribution. Sadly this adds no
weight to the quoted case report  which also omitted relevant
A case report needs the relevant data to allow a conclusive judgement
to be made!
 Goldstein LB et al. Charlson Index comorbidity adjustment for
ischaemic stroke outcome studies. Stroke 2004;35:1941-5
 Riggs JE. Neurological manifestations of electrolyte
disturbances. Neurol Clin. 2002;20(1):227-239
 Jones S, Iyadurai P, Chung SS. New onset seizure in adults:
Possible association with consumption of popular energy drinks