Subarachnoid pharmacotherapy, a novel therapeutic strategy for the treatment of focal neocortical epilepsy, could be adapted for the treatment of stroke. Specifically, subarachnoid pharmacotherapy could be adapted to maximize functional recovery after cortical ischemic stroke. The key element of this strategy is a device im-planted chronically in the subarachnoid space overlaying the cortical infarct and penumbra. The triple functions of this device are: (a) periodic transmeningeal drug delivery to promote neuroregeneration in the penumbra without causing damage by penetration into the cortical tissue, (b) periodic removal of accumulated inflammato-ry cells and molecules from the drug delivery site to prevent clogging in the drug delivery system, and (c) period-ic detection of local EEG signals to monitor the efficacy of the subarachnoid drug treatment and to help to optim-ize drug delivery/fluid removal parameters. All functions of the device are regulated by a connected control im-plant. Preliminary safety studies in bonnet macaques not subjected to experimental stroke showed that the subarachnoid device is well tolerated and can perform its triple functions for months without causing apparent neurological or behavioral abnormality. Relevant efficacy tests in animal models of cortical ischemic stroke are needed to predict the clinical potential of subarachnoid pharmacotherapy for post-stroke recovery.

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