The interaction between microtubule organizing centers (MTOCs) and spindle poles is critical for the establishment and maintenance of the mitotic apparatus in many organisms. However, our understanding of the dynamics of this relationship and the potential implications for tissue homeostasis remains largely unexplored. Here we report that the microcephaly-associated protein, Abnormal Spindle (Asp), plays a key role in maintaining centrosome-pole attachments and pole focusing in Drosophila neural stem cells. Complete loss of function mutations in asp cause centrosome detachment from poles shortly after metaphase, leading to free-ranging centrosomes that randomly move around the cell until anaphase onset. As a consequence, centrosome inheritance is randomized, with neural stem cells either losing their centrosome or retaining both following asymmetric division. Furthermore, we show that Asp’s spindle function is dependent on the calcium-sensing protein Calmodulin (CaM). Both proteins colocalize on spindles and dynamically move towards spindle poles with similar velocities, suggesting that they form a complex with CaM acting as a regulator of Asp. Our direct binding assay and structure-function analysis of Asp support this hypothesis. However, the Asp-CaM interaction is dispensable for head and brain size, and the spindle defects observed in neural stem cells of asp mutants do not correlate with microcephaly phenotypes. Instead, the ability of Asp to suppress microcephaly is conferred by an unknown domain in the N-terminus of the protein through a mechanism that is currently under investigation.