Infection with the Zika virus is known to cause the devastating birth defect microcephaly, marked by neurological problems and a smaller than normal brain. Zika has also been linked to another neurological disorder, Guillain-Barré syndrome, in which the body's immune system attacks part of the nervous system, causing weakness, tingling, and sometimes paralysis.
But as knowledge about the Zika virus grows, it appears the virus can potentially trigger other neurological woes — including a syndrome that mimics severe symptoms of multiple sclerosis (MS).
At the recent American Academy of Neurology meeting in Vancouver, Maria Lucia Brito Ferreira, MD, presented cases of patients with symptoms of infection with mosquito-borne arboviruses (which include Zika, dengue fever, yellow fever, and chikungunya) who developed the type of neurologic problems seen in some autoimmune disorders, including MS.
Between December 2014 and June 2015, Ferreira and her colleagues at Restoration Hospital in Recife, Brazil, saw 151 patients with Zika-type symptoms. All were admitted to the hospital with fever followed by a rash. Some had red eyes, and many suffered from severe itching and muscle and joint pain.
Six developed autoimmune-type neurological manifestations, either immediately or as late as 15 days after their Zika virus symptoms started. Tests showed all of these patients were infected with Zika but none had contracted the dengue and chikungunya viruses. So Zika virus appeared to be the smoking gun behind the patients’ worrisome nervous system and brain-related symptoms — some of which turned out to be surprising.
Two of the patients developed acute disseminated encephalomyelitis (ADEM). This potentially serious neurological illness is characterized by a brief attack of widespread inflammation in the brain and spinal cord that damages myelin, the covering that protects nerve fibers. In fact, brain imaging revealed the white matter in these patients’ brains had been damaged — results similar to those found in brain scans of many people with MS. Fortunately, people with ADEM, unlike in MS, typically suffer only from one bout of the disease, and most recover in six months or less.
Four of the patients with Zika who were followed by Ferreira and fellow doctors developed Guillain-Barré syndrome, which also affects myelin in the nervous system.
When they were well enough to leave the hospital and go home, five of the six Zika patients who had developed neurological symptoms were still having difficulty with motor functioning, such as muscle weakness. One patient had continued thinking and memory problems, and another had vision difficulties.
“This doesn’t mean that all people infected with Zika will experience these brain problems,” Ferreira emphasized. “Of those who have nervous system problems, most do not have brain symptoms. However, our study may shed light on possible lingering effects the virus may be associated with in the brain.”
While much more research is needed to pinpoint how Zika may be causing neurological problems, Raad Shakir, MD, president of the World Federation of Neurology, wrote in a commentary published in The Lancet Neurology that neurological expertise is needed to deal with the potential neurological problems Zika may cause.
“At present, it does not seem that ADEM cases are occurring at a similarly high incidence as the Guillain-Barré syndrome cases, but these findings from Brazil suggest that clinicians should be vigilant for the possible occurrence of ADEM and other immune-mediated illnesses of the central nervous system,” said CDC neurologist and epidemiologist James Sejvar, MD.
“Of course, the remaining question is ‘why’ — why does Zika virus appear to have this strong association with Guillain-Barré syndrome and potentially other immune/inflammatory diseases of the nervous system? Hopefully, ongoing investigations of Zika virus and immune-mediated neurologic disease will shed additional light on this important question.”
June 06, 2016
Christopher Nystuen, MD, MBA