Monday, 6 June 2016

Post viral cerebellar ataxia

Post viral cerebellar ataxia

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Post-viral cerebellar ataxia (ACA) also known as acute cerebellitis is a disease characterized by the sudden onset of ataxia following a viral infection.[1] The disease affects the function or structure of the cerebellum region in the brain.


Since the majority of ACA cases result from a post-viral infection, the physician’s first question will be to ask if the patient has been recently ill. From this point a series of exclusion tests can determine if the current state of ataxia is a correct diagnosis or not. A CT (computed tomography) scan with normal results can rule out the possibility of the presence of a posterior fossa tumor and an acute hemorrhage, which would both have abnormal results. Other imaging tests like EEG (electroencephalographs) and MRI (magnetic resonance imaging) can also be performed to eliminate possible diagnoses of other severe diseases, such as neuroblastoma, drug intoxication, acute labyrinthitis, and metabolic diseases. A more complicated test that is performed for research analysis of the disease is to isolate viruses from the CSF (cerebrospinal fluid). This can show that the virus has attacked the nervous system of the patient and resulted in the ataxia symptoms.[citation needed]

Differential Diagnosis[edit]

Differential diagnosis may include:


Most symptoms of people with post-viral cerebellar ataxia deal to a large extent with the movement of the body. Some common symptoms that are seen are clumsy body movements and eye movements, difficulty walking, nausea, vomiting, and headaches.[citation needed]


Post-viral cerebellar ataxia is caused by damage to or problems with the cerebellum. It is most common in children, especially those younger than age 3, and usually occurs several weeks following a viral infection. Viral infections that may cause it include the following: chickenpox, Coxsackie disease (viral infection also called hand-foot-and-mouth disease), Creutzfeldt-Jakob disease (a rare disease believed to be an infection that causes mental deterioration), Lyme disease (inflammatory bacterial disease spread by ticks), mycoplasma pneumonia (type of bacterial pneumonia), Epstein-Barr Virus (a common human virus that belongs to the herpes family) and HIV.[2]


Ataxia usually goes away without any treatment. In cases where an underlying cause is identified, your doctor will treat the underlying cause. In extremely rare cases, you may have continuing and disabling symptoms. Treatment includes corticosteroids, Intravenous immunoglobulin, or plasma exchange therapy. Drug treatment to improve muscle coordination has a low success rate. However, the following drugs may be prescribed: clonazepam, amantadine, gabapentin, or buspirone. Occupational or physical therapy may also alleviate lack of coordination. Changes to diet and nutritional supplements may also help. Treatment will depend on the cause. If the acute cerebellar ataxia is due to bleeding, surgery may be needed. For a stroke, medication to thin the blood can be given. Infections may need to be treated with antibiotics. Steroids may be needed for swelling (inflammation) of the cerebellum (such as from multiple sclerosis). Cerebellar ataxia caused by a recent viral infection may not need treatment.[citation needed]

Outlook (Prognosis)[edit]

People whose condition was caused by a recent viral infection should make a full recovery without treatment in a few months. Fine motor skills, such as handwriting, typically have to be practised in order to restore them to their former ability. In more serious cases, strokes, bleeding or infections may sometimes cause permanent symptoms.[citation needed]


Westphal reported the first documented case of post-viral cerebellar ataxia in 1872, where associations of reversible cerebellar syndrome were observed.[3] Another early case was documented in 1905. Batten described in detail cases of post-infectious cerebellar ataxia in five children. The cause of the disease was unknown until 1978 when Weiss and Guberman proposed that ACA could be due to direct invasion of the central nervous system by infectious agents. Since then many case studies have followed to understand the underlying conditions, symptoms and causes of the disease. The largest study of retrospective childhood ACA was done in 1994 by Connolly. This disease is still commonly used as a reference in clinical practice for other inflammatory and autoimmune disorders of the nervous system.[4]


  1. Jump up ^ Nussinovitch, Moshe; Prais, Dario; Volovitz, Benjamin; Shapiro, Rivka; Amir, Jacob (2003). "Post-Infectious Acute Cerebellar Ataxia in Children". Clinical Pediatrics 42 (7): 581–4. doi:10.1177/000992280304200702. PMID 14552515. 
  2. Jump up ^ Bergquist, Jennifer (September 12, 2005). "Childhood Ataxia" (PDF). University of Chicago. Retrieved 7 September 2012. 
  3. Jump up ^ Hinchey, Judy; Chaves, Claudia; Appignani, Barbara; Breen, Joan; Pao, Linda; Wang, Annabel; Pessin, Michael S.; Lamy, Catherine; Mas, Jean-Louis; Caplan, Louis R. (1996). "A Reversible Posterior Leukoencephalopathy Syndrome". New England Journal of Medicine 334 (8): 494–500. doi:10.1056/NEJM199602223340803. PMID 8559202. 
  4. Jump up ^ Bae, Jong Seok; Kim, Byoung Joon (2005). "Cerebellar ataxia and acute motor axonal neuropathy associated with Anti GD1b and Anti GM1 antibodies". Journal of Clinical Neuroscience 12 (7): 808–10. doi:10.1016/j.jocn.2004.09.019. PMID 16054817. 

Further reading[edit]

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