**5. Variability in rate or progression**

The ataxia disorders may be associated with very specific causes. When the onset of symptoms occurs acutely and abruptly, it may be related to vascular and/or structural brain damage. While rapid onset over hours-days is more associated with infectious or parainfectious cerebellitis, immune-mediated diseases such as Miller–Fisher syndrome, acute exposure to toxins, metabolic insult, or multiple sclerosis [27, 28]. Onset that occurs over weeks to months is associated with paraneoplastic disorders: anti-glutamic acid decarboxylase antibody syndrome, steroid-responsive encephalopathy and ataxia, gluten ataxia in celiac disease, vitamin deficiency states, general medical conditions such as hepatic encephalopathy, infections, sensory polyneuropathy, and ganglionopathy.

The long-standing progression occurring over the years is associated with genetic ataxias and may vary according to the individual: toxins, multiple sclerosis, storage disorders, sporadic neurodegenerative disorders, atypical parkinsonian conditions such as progressive supranuclear palsy or neurosyphilis. All possible etiologies must be considered when the clinical course is not fully determined. They must be differentiated from disorders such as dystonia, parkinsonism, chorea, myoclonus, cognitive impairment, pyramidal signs, sensory loss, hyporeflexia, cognitive and psychiatric symptoms, eye movement abnormalities, visual loss, neuromuscular deficits, telangiectasias, Achilles xanthomas, and early cataracts [30].
