| 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)
|
|
|
- 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
|
|
|
|
|
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| Vestibular neuritis
|
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