Differential diagnosis There are several other disorders with similar symptoms or laboratory features that physicians may consider when diagnosing A–T. The three most common disorders that are sometimes confused with A–T are: Cerebral palsy Friedreich's ataxia Cogan oculomotor apraxia Each of these can be distinguished from A–T by the neurologic exam and clinical history. Cerebral palsy (CP) describes a non-progressive disorder of motor function stemming from malformation or early damage to the brain. CP can manifest in many ways, given the different manner in which the brain can be damaged; in common to all forms is the emergence of signs and symptoms of impairment as the child develops. However, milestones that have been accomplished and neurologic functions that have developed do not deteriorate in CP as they often do in children with A–T in the late pre-school years. Most children with ataxia caused by CP do not begin to walk at a normal age, whereas most children with A–T start to walk at a normal age even though they often "wobble" from the start. Pure ataxia is a rare manifestation of early brain damage or malformation, however, and the possibility of an occult genetic disorder of brain should be considered and sought for those in whom ataxia is the chief manifestation of CP. Children with ataxic CP will not manifest the laboratory abnormalities associated with A–T. Cogan occulomotor apraxia is a rare disorder of development. Affected children have difficulty moving their eyes only to a new visual target, so they will turn their head past the target to "drag" the eyes to the new object of interest, then turn the head back. This tendency becomes evident in late infancy and toddler years, and mostly improves with time. This contrasts to the oculomotor difficulties evident in children with A–T, which are not evident in early childhood but emerge over time. Cogan's oculomotor apraxia is generally an isolated problem, or may be associated with broader developmental delay. Friedreich ataxia (FA) is the most common genetic cause of ataxia in children. Like A–T, FA is a recessive disease, appearing in families without a history of the disorder. FA is caused by mutation in the frataxin gene, most often an expansion of a naturally occurring repetition of the three nucleotide bases GAA from the usual 5–33 repetitions of this trinucleotide sequence to greater than 65 repeats on each chromosome. Most often the ataxia appears