Three cases of movement disorders secondary to hypoxic-ischemic encephalopathy are reported. Despite similarities among the clinical events, the neurological syndromes produced were dissimilar. Cerebral hypoxia-ischemia typically produces lesions of the globus pallidus that may result in an akinetic rigid syndrome. Due to its unique blood supply, vascular insufficiency is found to be a major factor. Lesions in the putamen also occur, and these tend to be associated with dystonia. Recent evidence supports a specific neuronal sensitivity in the striatum, possibly due to afferent excitatory amino acid connections. These two components and changes in the levels of neurotransmitters during hypoxia-ischemia may interact to produce varied clinical outcomes. These factors must also be considered when planning therapeutic interventions.