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Drug-induced ataxia
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Drug-induced ataxia

Contributors: Jennifer Vermilion MD, Christine Osborne MD, Richard L. Barbano MD, PhD
Other Resources UpToDate PubMed


Medications and toxins can lead to a transient or permanent ataxia, which may be cerebellar or sensory in origin. Cerebellar ataxia can present with a wide-based and unsteady gait, impaired dexterity, abnormal eye movements (nystagmus), a scanning dysarthria, or a combination of these findings. A thorough medication history should be obtained in ataxic patients without a readily apparent cause. Commonly implicated medications include:

Antiepileptic drugs
  • Phenytoin – May cause nystagmus at therapeutic doses, but ataxia is common at supratherapeutic levels. Effects are typically reversible with medication cessation, but permanent cerebellar degeneration can occur with chronic administration.
  • Valproic acid – May cause cerebellar ataxia in the setting of hyperammonemia.
  • Benzodiazepines – Most commonly described in children with epilepsy. Ataxia is often mild and reversible. Elderly patients are also susceptible to benzodiazepine ataxia.
  • Others – Carbamazepine, oxcarbazepine, lacosamide, lamotrigine, rufinamide, zonisamide, ezogabine, gabapentin, felbamate, and phenobarbital.
Psychiatric medications
  • Chronic lithium use is associated with ataxia that is often permanent. Symptom onset tends to occur after infection, dehydration, or renal dysfunction.
  • Ataxia secondary to selective serotonin reuptake inhibitor use has been reported.
Chemotherapeutic and immunosuppressive agents
  • Tacrolimus and cyclosporine are associated with mild and transient ataxia.
  • Cytarabine-induced ataxia tends to occur 2-4 days after first dose and typically resolves within weeks.
Antimicrobials – Ataxia typically resolves with removal of the drug.
  • Metronidazole – High doses associated with ataxia and development of cerebellar hyperintensities in T2 sequences on MRI.
  • Piperazine (antihelmintic agent) can cause ataxia in children.
  • Most common toxin producing ataxia in a midline cerebellar pattern, characterized by ataxia of the legs and gait with relative sparing of the arms.
Other toxins and poisons
  • Carbon tetrachloride, heavy metals, phencyclidine (PCP), and toluene may cause cerebellar ataxia.
Sensory ataxia can arise secondary to a peripheral neuropathy. Like cerebellar ataxia, sensory ataxia may present with a wide-based and unsteady gait. In addition, individuals have a positive Romberg sign. They may have a high-stepping gait due to motor weakness or a foot-slapping gait due to loss of sensation.

Medications commonly implicated in peripheral neuropathy include:

Cardiovascular agents
  • Statins and amiodarone may cause a reversible peripheral neuropathy.
Chemotherapeutic agents
  • Chemotherapy-induced peripheral neuropathy (CIPN) is a well-described entity and may be caused by various agents.
  • Vincristine, paclitaxel, cisplatin, and bortezomib are common causes of CIPN.
  • Isoniazide can cause a reversible peripheral neuropathy.
  • Metronidazole may cause a reversible peripheral neuropathy.
Antiretroviral therapy (ART)
  • Nucleoside reverse transcriptase inhibitors such as stavudine contribute to polyneuropathy in patients with human immunodeficiency virus (HIV).
  • Vitamin B6 (pyridoxine) in high doses can cause peripheral neuropathy. However, pyridoxine supplementation can prevent neuropathy in patients on isoniazid therapy.


R27.0 – Ataxia, unspecified

20262006 – Ataxia

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Last Reviewed:12/18/2018
Last Updated:10/28/2021
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Drug-induced ataxia
A medical illustration showing key findings of Drug-induced ataxia : Nystagmus
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