Eliciting percepts akin to natural vision using brain computer interfaces is the holy grail of vision prosthetics. However, progress has been slowed by our lack of understanding of how the human visual cortex processes and encodes information as well as how external perturbations, such as electrical stimulation via multi-electrode arrays, might perturb the recurrent cortical dynamics. Furthermore, investigating these questions directly remains difficult as we rarely have the opportunity to probe the human cortex in-vivo. From this limitation and thanks to the current exponential increase in computing capabilities, modeling and simulation tools naturally came to complement experimental studies. However, while biophysically detailed brain models, such as the ones developed by the Allen Institute for Brain Science [1] or the Blue Brain Project [2], would be ideal to study the dynamics of the visual cortex under the influence of external perturbations, are now available, they stay prohibitively expensive to run to simulate long stimulation protocols, and more importantly are built to reproduce rodents, which have substantially different organization of visual system to humans, lacking for example the columnar organization of visual features. We present here a model of intracortical microstimulation (ICMS) applied to a model of columnar primary visual cortex (V1) [3]. The V1 model, built from computationally cheap but versatile point neuron models, contains functional retinotopy and orientation maps which are both essential for studying the interaction between external drives such as ICMS and structured spontaneous dynamics. The present modeling of ICMS follows a data-driven approach and aims to maintain a balance between modeling pertinent biological details when necessary and using phenomenological simplifications whenever possible. To achieve this balance we aimed at reproducing two of the main features of ICMS: the sparse and distributed statistics with which microelectrodes recruit neurons and the ectopic spikes induced in the activated neurons. We demonstrate that our model reproduces the stereotypical dynamics in V1 seen as a response to ICMSs.