**3.6 Secondary ataxia**

Ataxias caused by exogenous or endogenous nongenetic factors, such as those that are toxic, paraneoplastic, immune-mediated, nutritional, and infectious in character, as well as localized damage to the cerebellum, fall under the category of secondary or acquired ataxias [26, 29, 30]. When characterizing localized lesions in the cerebellum and its connections due to conditions including neoplastic, inflammatory, demyelinating, and vascular illnesses, neuroimaging investigations are crucial [26, 29, 30]. The unfavorable effects of some medications might also cause ataxia [39]. Whereas, antiepileptic drugs like oxcarbazepine, lamotrigine, and phenytoin, benzodiazepines like nitrazepam and triazolam, and antineoplastic/immunosuppressive medications like cytarabine, tacrolimus, and cyclosporine are the most prevalent causes of druginduced cerebellar ataxia [39]. Ataxia can also be brought on by chemicals including alcohol, lithium, and toluene [39, 40]. Otherwise, cerebellar ataxia can result from a number of infectious diseases, including syphilis, Whipple's disease, the mumps, and infectious mononucleosis [26, 29, 30]. It can also be a symptom of endocrine disorders, notably hypothyroidism. Hashimoto's encephalopathy, also known as a steroidresponsive encephalopathy, is associated with autoimmune thyroiditis (Thomas [26, 29, 30]). Whereas, it has been reported that people who do not get enough vitamins including thiamine, tocopherol, and cobalamin may develop cerebellar and afferent/ sensory ataxias [26, 29, 30]. While antibodies against glutamic acid decarboxylase (GAD), which were first identified in individuals with stiff-person syndrome, have also been linked to cerebellar ataxia [26, 29, 30, 41, 42]. A body of evidence sustain a sex dimorphism of such immune-mediated cerebellum condition, with women being more likely to have anti-GAD ataxia, which can also coexist with thyroid disorders and insulin-dependent diabetic mellitus. While intravenous immunoglobulins and steroids have varying effects on anti-GAD ataxia. Otherwise, gluten ataxia is another immune-mediated condition brought on by gluten consumption in people with a genetic predisposition [43]. The disease is characterized by adult-onset, progressive gait ataxia with gaze-evoked nystagmus and peripheral neuropathy symptoms. In all cases, the anti-gliadin antibody is positive and an anti-gluten diet can enhance gluten ataxia [43].
