The literal meaning of the Greek term ‘apraxia’ is ‘without action’. Apraxia in behavioral neurology refers to the loss of the ability to carry out learned, skilled actions (e.g. opening door with a key) in the absence of motor, sensory, coordination or comprehension abnormalities. It is to be differentiated from akinesia, which is defined as a general failure to initiate movement in the absence of weakness. For the desired motor function to occur, it goes through three distinct phases: ideation, planning, and execution. Structures involved in praxis are mainly in the dominant parietal cortex, frontal cortex, basal ganglia, and corresponding white matter connecting these areas. Spatiotemporal movement formulas or visual-kinesthetic motor engrams, also known as praxicons, are essential for skilled learned movements. Activation of these models can be visual, auditory, verbal, or tactile—a model for praxis based on the work of Heilman and Rothi. Neurons in the inferior parietal cortex fire selectively to initiate the process of praxis after recognition of the input provided, especially in left parietal sub-regions. In 1920, Liepmann suggested 3 different types: limb-kinetic apraxia, ideomotor apraxia, and ideational apraxia. Whether all of these are in fact disorders of ‘skilled action’ is debatable. This controversial nature of apraxia is also reflected in the highly variable rules behind naming of apraxia types and apraxic phenomena. Some are named based upon the body parts involved (e.g. orofacial, ocular motor), some are named after their putative mechanisms (e.g. ideational, constructional), others are named after the tasks that are involved (e.g. writing, speech, eyelid opening), and in rare cases, naming involves the neuroanatomical substrate (e.g. callosal apraxia). CAS is a neurological childhood (pediatric) speech sound disorder in which the precision and consistency of movements underlying speech are impaired in the absence of neuromuscular deficits (e.g. abnormal reflexes, abnormal tone. CAS may occur as a result of known neurological impairment, in association with complex neurobehavioral disorders of known and unknown origin, or as an idiopathic neurogenic speech sound disorder. The impairment in planning and/or programming spatiotemporal parameters of movement sequences results in errors in speech sound production and prosody.