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Zika Virus Associated with Acute Disseminated Encephalomyelitis and Guillain-Barre Syndrome


I know I said I wasn’t going to post about Zika virus because there were so many bigger sites making daily posts, but I found one new piece of information that was especially interesting.  The American Academy of Neurology issued a press release on Friday, April 15 about a case study of patients admitted to the Restoration Hospital in Recife, Brazil between December 2014 and June 2015.  Six patients with Zika virus developed neurological symptoms: four with Guillain-Barre Syndrome (GBS) and two with acute disseminated encephalomyelitis (ADEM).

All the patients had symptoms of Zika virus infection, including fever, rash, sometimes severe itching, joint and muscle pain, and conjunctivitis (red eyes.)  Neurological symptoms developed immediately or within fifteen days after infection.

Two of the patients had symptoms of ADEM: headache, severe weakness, numbness, and impairment of consciousness, sometimes associated with visual loss.  Symptoms of ADEM are similar to those of multiple sclerosis (MS), although in ADEM complete or near-complete recovery is usually seen within six months, whereas in MS, there are repeated and progressive attacks.  In addition, in ADEM, there is usually impairment of consciousness during the initial attack.

Four of the patients described had symptoms of GBS: tingling or numbness that begins in the feet and spreads upwards, weakness that spreads similarly, severe pain like aches or cramps, especially in the back, ataxia (difficulty and unsteadiness in walking), weakness of eye, facial, speaking, swallowing muscles,  difficulty with bowel and bladder function, rapid heart rate, difficulty breathing, and unstable blood pressure.

Oddly, both of these disorders can also be associated with immunizations, such as mumps-measles-rubella (MMR) shots.  They are both believed to be autoimmune disorders.  ADEM shows up in MRI scans as white-matter changes, somewhat similar to those seen in MS.  GBS is diagnosed by spinal tap that shows elevated immune proteins, although the clinical symptoms are usually considered diagnostic.

These conditions are both signs of abnormal immune reactions to the Zika infection that cause immune proteins to attack the myelin that coats and insulates nerve fibers.  Loss of myelin causes nerves to lose their ability to transfer signals rapidly, so signals are weaker and slower than normal.  Abnormal nerve signalling causes neurological symptoms– the constellation of symptoms we have just described.

What makes these syndromes relevant is the connection to fetal injuries from Zika virus infection: the fetal damage is neurological, primarily to the central nervous system.  There may also be damage to the fetal peripheral nervous system but this has not been studied yet.  There may be a common cause of fetal and adult syndromes in Zika infection.  The conditions may both be mediated by immunological reaction to the infection, a hypothesis that has yet to be evaluated.

The neurological syndrome descriptions above were taken from two web sites: the National Institutes of Health information pages for ADEM, and the Medscape pages on GBS.

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