Cell delamination is a conserved morphogenetic process important for generation of cell diversity and maintenance of tissue homeostasis. Here we used Drosophila embryonic neuroblasts as a model to study the apical constriction process during cell delamination. We observe dynamic myosin signals both around the cell adherens junctions and underneath the cell apical surface in the neuroectoderm. On the cell apical cortex the non-junctional myosin forms flows and pulses, which are termed as medial myosin pulses. Quantitative differences in medial myosin pulse intensity and frequency are critical to distinguish delaminating neuroblasts from their neighbors. Inhibition of medial myosin pulses blocks delamination. The fate of neuroblasts is set apart from their neighbors by Notch signaling-mediated lateral inhibition. When we inhibit Notch signaling activity in the embryo, we observe that small clusters of cells undergo apical constriction and display an abnormal apical myosin pattern. Together, we demonstrate that a contractile actomyosin network across the apical cell surface is organized to drive apical constriction in delaminating neuroblasts.