A 2-month-old girl presented for neurologic evaluation secondary to mild facial dysmorphism, feeding difficulties, and failure to thrive. She was born at 39 weeks gestation following an uncomplicated pregnancy and delivery, with a birth weight of 2155 grams (small for gestational age). Documented at physical examination were a large anterior fontanel, a prominent and wrinkled forehead, a wide nasal bridge, low-set ears, upturned nares, and a sacral dimple. Magnetic resonance imaging of the lumbosacral plexus was consistent with a low-lying conus and a tethered spinal cord. Cranial magnetic resonance imaging (Fig 1) showed complete absence of sulcation with a smooth brain surface consistent with classical (Type I) lissencephaly. Electroencephalography indicated low-amplitude background activity over the posterior head regions, also consistent with lissencephaly. Chromosomal analysis revealed a deletion of the terminal region of the short arm of chromosome 17 (17p13.3), which contains the LIS1 gene (HGNC gene symbol PAFAH1B1) gene (alias LIS1), consistent with Miller-Dieker syndrome. Parental chromosomal findings were normal, indicating a de novo deletion. Transthoracic echocardiography yielded normal findings. She developed problems with gastroesophageal reflux, aspiration, and partial complex seizures by 3 months of age. By 6 months of age, she was noted to have distended forehead veins, central hypotonia, global developmental delay, and clusters of seizures suggestive of infantile spasms. Electroencephalography indicated frequent multi-