Ataxia differential diagnosis

TYPE	CAUSE	PROGRESSION	IMAGING FEATURES and OTHER TESTS	ASSOCIATED FACTORS	SYMPTOMS
Acute cerebellitis	Primary infectious, postinfectious or postvaccination disorder. Epstein-Barr virus, influenza A and B, mumps, varicella-zoster virus, coxsackie virus, rotavirus, echovirus, Mycoplasma pneumoniae and immunization	From self-limited to fatal, depending on the amount of cerebellar swelling	Normal or abnormal brain magnetic resonance imaging (MRI) at onset Bilateral hemispheric cerebellar swelling with cortical and white matter T2 hyperintensities; leptomenigeal enhancement may be present. CSF: Elevated protein and leukocytes, with lymphocytic predominance, normal glucose Blood/CSF: Antibodies anti- HSV, EBV, VZV, mumps, rubella, Lyme disease	Postinfectious cerebellitis typically occurs between one and six weeks after varicella or measles, but also can follow Epstein-Barr or other viral infections and vaccinations in teenagers and young adults.	Trunk and limbs ataxia, fever, abnormal eye movements, dysarthria, headache, nausea, vomiting and decreased level of consciousness
Bacterial infection	Mycoplasma pneumoniae, Listeria monocytogenes		Lumbar puncture for examination of the cerebrospinal fluid (CSF) and microbiologic testing		Fever instability when walking changes in coordination that primarily affect the trunk or head and not the limbs nodding or other unusual head movements unusual eye movements, such as involuntarily darting from side to side slow or slurred speech changes in mood, behavior, or personality headaches nausea or vomiting
Acquired immunodeficiency syndromes	Related to M. pneumonia, Epstein-Barr virus, herpes simplex virus, and toxoplasmosis	Subacute ataxia which progress in months	Positive serologic test for HIV Cerebellar atrophy
Chronic alcohol use/Alcoholic cerebellar degeneration	Toxic effects on the central and peripheral nervous systems Direct toxic alcoholic effect on the Purkinje cells	Rapid progression (weeks or months)	Vermis atrophy		Severe ataxia of gait and lower limbs with relatively mild involvement of the upper limbs. Speech and ocular motility are usually preserved
Antibiotic-induced acute ataxia	Interaction of polymyxins with neurons has been associated with the occurrence of several neurotoxic events	Weeks after initiation	Brain MRI abnormalities Characteristic reversible MRI signal abnormalities in the cerebellar dentate nuclei, dorsal brainstem, or splenium of the corpus callosum Non-specific EEG abnormalities		Ataxia may also occur in isolation or combined with dizziness, generalized muscle weakness, partial deafness, visual disturbances, vertigo, confusion, hallucinations, seizures, and neuromuscular blockade
Toxic ingestions	Alcohol, benzodiazepines, or other anticonvulsant drugs or exposure to environmental toxins such as mercury or lead		Toxicology testing Elevated plasma levels of substances like lithium, and phenytoin Other imaging unremarkable; Cerebellar atrophy in late stages		Additional findings that suggest occult ingestion (eg, depressed consciousness)
Atypical infections	Progressive multifocal leukoencephalopathy	Progressive and multifocal	Magnetic resonance imaging (MRI) reveals a multifocal process limited to the white matter	Caused by reactivation of the JC virus in immunocompromised hosts.	Presents with subacute neurologic deficits like altered mental status, motor deficits (hemiparesis or monoparesis), limb ataxia, gait ataxia, and visual symptoms such as hemianopia and diplopia
Brain tumors	Nonmalignant and malignant tumors of the brain and spinal cord.				Symptoms and signs of tumor local invasion, Adjacent structures compression, Raised intracranial pressure
Stroke
Vestibular neuritis

References

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