 Specific manifestations of ataxia may correspond to certain causes or may be discovered by particular triggers. For example, truncal ataxia is typical of cerebellar vermian pathology [1]. A lurching gait, when triggered by head rotation, is typical of vestibular dysfunction [9]. Sensory ataxia can be revealed by a positive Romberg test, which examines the dorsal columns. [9]. Additionally, ataxia with specific signs can suggest the underlying disorder. Pupillary abnormalities may suggest drug or toxin ingestion versus third cranial nerve compression. Torticollis or resistance to head and neck motion may indicate pathology at the craniocervical junction, cord compression, or posterior fossa tumor [9]. Based on a systematic review of European data, the estimated prevalence of childhood ataxia due to genetic and acquired causes is approximately 26 per 100,000 children, although the true worldwide prevalence may be higher [10]. Regional variations exist in the prevalence of childhood ataxia, with a higher prevalence of genetic causes of ataxia in countries with high consanguinity, and a higher prevalence of infectious causes such as malaria and varicella in other regions where these diseases are more common [10]. Evaluation of ataxia requires careful review of demographics, history (especially duration of symptoms and the presence of additional neurological deficits), clinical examination, laboratory testing, and neuroimaging to reach a cohesive diagnosis [2,7,11-13]. In young children and infants, a detailed neurological examination is often challenging, and initial imaging therefore plays a critical role in arriving at a diagnosis. The time course of illness (eg, acute, recurrent, chronic with or without progression) may indicate or rule out potential etiology. Acute onset ataxia typically refers to ataxia that develops within hours or days and frequently presents within 72 hours, whereas chronic ataxia is defined as ataxia lasting longer than 2 months [1,14].
Ataxia Child.  Specific manifestations of ataxia may correspond to certain causes or may be discovered by particular triggers. For example, truncal ataxia is typical of cerebellar vermian pathology [1]. A lurching gait, when triggered by head rotation, is typical of vestibular dysfunction [9]. Sensory ataxia can be revealed by a positive Romberg test, which examines the dorsal columns. [9]. Additionally, ataxia with specific signs can suggest the underlying disorder. Pupillary abnormalities may suggest drug or toxin ingestion versus third cranial nerve compression. Torticollis or resistance to head and neck motion may indicate pathology at the craniocervical junction, cord compression, or posterior fossa tumor [9]. Based on a systematic review of European data, the estimated prevalence of childhood ataxia due to genetic and acquired causes is approximately 26 per 100,000 children, although the true worldwide prevalence may be higher [10]. Regional variations exist in the prevalence of childhood ataxia, with a higher prevalence of genetic causes of ataxia in countries with high consanguinity, and a higher prevalence of infectious causes such as malaria and varicella in other regions where these diseases are more common [10]. Evaluation of ataxia requires careful review of demographics, history (especially duration of symptoms and the presence of additional neurological deficits), clinical examination, laboratory testing, and neuroimaging to reach a cohesive diagnosis [2,7,11-13]. In young children and infants, a detailed neurological examination is often challenging, and initial imaging therefore plays a critical role in arriving at a diagnosis. The time course of illness (eg, acute, recurrent, chronic with or without progression) may indicate or rule out potential etiology. Acute onset ataxia typically refers to ataxia that develops within hours or days and frequently presents within 72 hours, whereas chronic ataxia is defined as ataxia lasting longer than 2 months [1,14].