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Thursday, February 11, 2016



A new study testing the benefits of a task-oriented rehabilitation program to strengthen hand and arm weakness on the heels of a stroke has called into question the belief that more hours of such an intensive training protocol is better than usual occupational therapy. Patients who received intensive upper-body training — 30 one-hour sessions over a 10-week period — fared no better than those who received a more standard type of rehabilitation, or the usual therapy with significantly fewer hours.  

Results of the study were published in the February 9 issue of the Journal of the American Medical Association.

Scientists at the University of Southern California in Los Angeles led the study, recruiting 361 stroke patients from seven hospitals around the country. The patients were randomly assigned to receive either one-hour intensive, structured upper-extremity training three times a week during the 10-week study; 30 hours of usual occupational therapy; or occupational therapy that was monitored but with no prescribed amount of hours. The rehabilitation services were delivered in an outpatient setting.

Carolee J. Winstein, PhD, a professor of biokinesiology and physical therapy and her colleagues at the University of Southern California, measured upper-extremity motor function and recovery for a year. They reported in the JAMA study that there were no group differences in upper extremity motor performance. The intensive, task-oriented rehabilitation did not result in any significant benefits compared with the usual occupational therapy or monitored-only standard rehabilitation practice, whether the control patient received 11 hours or the equivalent 30 hours of treatment. In other words, a more intensive treatment protocol wasn't any better at restoring motor performance.

"These findings do not support superiority of this task-oriented rehabilitation program for patients with motor stroke and moderate upper extremity impairment," the study authors wrote.

The study counters other recent research that has suggested that higher doses of task-oriented upper-extremity training is better for stroke patients than standard occupational and physical therapy. The researchers acknowledged that changing practices among physical and occupational therapists could have accounted for the similar motor outcome identified in the study. Also, the variability in the hours of rehabilitation that patients received in the control arm of the study could have skewed the results, they said.

Still, the researchers concluded: "The findings from this study provide important new guidance to clinicians who must choose the best treatment for patients with stroke. The results suggest that usual and customary community-based therapy, provided during the typical outpatient rehabilitation time window by licensed therapists, improves upper extremity motor function and that more than doubling the dose of therapy does not lead to meaningful differences in motor outcomes."​

Look for more in-depth coverage and independent analysis of this study in an upcoming issue of Neurology Today.





Wednesday, February 10, 2016



A team of scientists at Harvard Medical School and the Broad Institute has identified a risk gene in the major histocompatibility complex (MHC) on chromosome 6 that could explain why some people develop schizophrenia.

The gene, C4, comes in many varieties and they showed in a number of elegant studies that it is involved with synaptic pruning. After looking at tens of thousands of DNA samples from schizophrenia patients and controls (collected through the Psychiatric Genomics Consortium,) as well as dozens of slides from autopsied brain tissue from people who died of schizophrenia and controls, the scientists found that people who have more copies of a particular form of the gene, C4A, are at higher risk for the debilitating brain disease.

The study appears in the January 27th issue of Nature.

In 2014, the MHC region showed up as the strongest genetic signal in a large meta-analysis of genome-wide association studies.  

Steven McCarroll, PhD, an associate professor of genetics at Harvard Medical School, was interested in unraveling this puzzle. The MHC region has hundreds of genes and he wanted to find functional alleles that may have a role in schizophrenia. Dr. McCarroll and his colleagues observed that the C4 locus (within the MHC) had many alleles that had not been characterized. They developed a new method to look at data from the genome-wide association study samples, and identified 15 different forms of C4A and C4B. Each had a variable number of copies.

Experiments on post mortem brains then indicated that these alleles powerfully affected the expression of C4A and C4B: the genetic effect was so strong that it explained 70 percent of the variation in gene expression levels, Dr. McCarroll said.

The C4 gene encodes for an immune protein, but scientists have known for a few years that some other complement proteins have another function in the brain: to help prune synapses tagged for removal. This pruning process is activated during development and then sets into high gear again during late adolescence. The scientists suspect that an overactive pruning process in adolescence (triggered by the gene variant) could explain the development of disordered thinking and psychosis.

The scientists said that the findings could lead to the development of targeted treatments to selectively lower C4 expression (in the brain) and prevent or reduce the overactive pruning that may be taking place in adolescents on the road to schizophrenia. 

"No one is suggesting that this is the cause of schizophrenia in all patients," said Dr. McCarroll. "What is intriguing though is the connection of a strong population-level genetic effect with a specific set of common alleles, and the way these alleles shape a biological process. We are hoping that this hypothesis — that problems with synaptic pruning may help explain why some people get schizophrenia — will get real legs and spark more research."

He added, "It will take years of work and converging evidence to understand the importance of this and how it fits into other risk factors and pathways."

Read the expanded story with commentary from independent experts in the March 3 print and online issue of Neurology Today.






Friday, February 5, 2016



Genetic researchers have reported preliminary data indicating that inherited mutations of the prion protein (PRNP) gene are not only far more widespread than previously thought, but also that only a few of these are highly penetrant and have the capacity to develop into full-fledged neurodegenerative disease. Moreover, it might be possible someday to use pharmaceutical approaches to limit the amount of the prion protein released in affected individuals, according to the January 20 report in Science Translational Medicine.

The research, which was coordinated at the MacArthur Lab at Massachusetts General Hospital, the Broad Institute of Harvard, and the Massachusetts Institute Technology (MIT), was spearheaded by a PhD student at the Broad Institute and the Biological and Biomedical Sciences Division at Harvard University.

Eric Vallabh Minikel was a software engineer and data analyst at MIT when his wife, Sonia Vallabh, PhD, tested positive for the mutant D178N cis 129M allele of PRNP. The same mutation caused her mother's death in 2010, and the two dedicated themselves to studying prion mutations. The specific variant is highly penetrant, with symptoms typically occurring at around 50 years of age.

The massive study involved a large number of collaborators, notably members of the Exome Aggregation Consortium, a coalition of investigators seeking to aggregate and harmonize exome sequencing data from a wide variety of large-scale sequencing projects. Its data set includes 60,706 unrelated individuals sequenced as part of various disease-specific and population genetic studies.

To determine the possible prevalence of known PRNP mutations in the general population, the researchers also examined data on 531,575 individuals provided by the direct-to-consumer genotypic service 23andMe. The investigators excluded data from individuals from families with known prion disease. The entire data set included 16,025 prion disease cases, 60,706 population control exomes, and those provided by 23andMe.

They found that the frequency of reportedly pathogenic PRNP variants was more than 30 times higher in controls than expected on the basis of disease incidence.

"A total of 65 percent of cases underwent PRNP open-reading frame sequencing, with 12 percent of all cases, or 18 percent, having a rare variant, which is consistent with an oft-cited estimate that 15 percent of cases of Creutzfeldt-Jakob disease are familial," said Minikel.

The research team reported that no more than about 29 individuals per million in the general population should harbor the most active high-penetrance prion disease–causing variants, and that about 17 cases in the ExAC database and 15 people in 23andMe data would have been expected to harbor such variants.

"Instead, we found that variants in PRNP occupy a broad spectrum, but with big differences in how bad they are," Minikel told Neurology Today. "Variants previously considered rare are actually pretty common in the general populations, yet the patients who have been told they have a PNRP mutation, and their lifetime risk of disease is 100 percent, may only have 1 percent or less risk."

Significantly, they found that three healthy older persons had just one non-functional prion gene allele and, unlike those with two, it means they likely had only half the normal amount of cellular prion protein, providing the first human genetic data on the effects of a 50 percent reduction in the degree of impact in such individuals.  No one has identified persons before with only one functional PRNP gene, which means, in theory, that it might be possible to safely reduce PRNP gene expression by 50 percent in other patients with prion disease.

"For the first time, this should answer the question of whether therapeutic agents to reduce PRNP expression may not only be effective, but also whether patients with penetrant variations might be treated safely — something that will require additional research," said Minikel.



The researchers found that missense variants in PRNP previously reported to be pathogenic are at least 30 times more common in the population than expected on the basis of genetic prion disease prevalence, and while some of this excess can be attributed to benign variants falsely assigned as pathogenic, others have genuine effects on disease susceptibility. In all, PRNP variants confer an estimated lifetime risks ranging from less than 1 percent to 100 percent, depending on the type and site of the mutation.

The team looked specifically at missense variations which occur when a change in a single nucleotide encodes for an abnormal protein, in this case PRNP.

The probability that a carrier of a suspected disease-causing genotype will develop disease has generally been, and continues to be uncharted territory, said Minikel, but researchers are increasingly developing a better understanding of penetrance.

"Although the number of individuals and the depth of available phenotype data were limited, and the lifetime inactivation of a gene is an imperfect model of the effects of pharmacological depletion of the gene product, the data provide preliminary evidence that a reduction in PRNP dosage, if achievable in patients, is likely to be tolerated," said Minikel.

In the general population, of all persons with these variants, most will not develop prion disease and only one half of individuals with a family member who develop disease have penetrant versions.

"For most individuals there is only a very small risk, however there are those with much higher risk," he noted.

Increasingly large exome sequencing data sets will soon enable researchers to test whether the same is true of other genes currently being targeted in substrate-reduction therapeutic approaches for other protein-misfolding disorders, he continued.

"Together, our findings highlight the value of large reference data sets of human genetic variation for informing both genetic counseling and therapeutic strategy. I hope that what we have done might be possible with other genetic dominant neurodegenerative diseases, and that we will see more efforts like this," Minikel told Neurology Today.

"We did not predict that we would discover these findings because all PRNP variants were thought to convey pathogenic risk. For 10 years or so, researchers have been investigating ways to address PRNP using small molecules to counter expression of PRNP and tests in mice gave shown they can reduce protein levels, which is also promising. As exome data sets increase, we will get more information about PRNP phenotypes and penetrance."



James Mastrianni, MD, PhD, an associate professor of neurology and director of the Center for Comprehensive Care & Research on Memory Disorders at the University of Chicago, told Neurology Today that the findings are important for several reasons.

"The paper highlights a key problem associated with genetic studies of rare disorders like prion disease," said Dr. Mastrianni, the Helen McLoraine Neuroscientist at the Brain Research Foundation, a public, nonprofit, charitable organization that provides funding for investigators.

"Although, only a handful of mutations of the PRNP are clearly causal, based on linkage analysis, there are well over 30 rare mutations of PRNP that have been associated with disease and are often considered causal, but family history is either lacking or spotty. Some mutations even appear to be age-dependent, often appearing in patients who develop CJD late in life."

He said that Minikel and his colleagues took advantage of newly available large genetic databases and found a much higher prevalence of some mutations in control populations that would be expected in such a rare disease.

"They then assigned some much needed lifetime risk numbers, which could be valuable in genetic counseling. The study is an important reminder to those in the field that caution is advised about casually assigning cause to a genetic variant of a rare disease," he stated.

"The investigators' incidental recognition of a few asymptomatic individuals with heterozygous loss-of-function due to PRNP variants also gives hope to those of us who are applying RNA interference to knock down expression of the mutates allele as a potential therapy for genetic prion disease."




·      Minikel EV, Vallabh SM, Lek M, et al. Quantifying prion disease penetrance using large population control cohorts. Sci Transl Med 2016:8:322ra9.


·      Prusiner SB, Woerman AL, Mordes DA, et al. Evidence for alpha-synuclein prions causing multiple system atrophy in humans with parkinsonism. PNAS 2015:112:E5308-E5317.


·      Jansen C, Parchi P, Capellari S, et al. Prion protein amyloidosis with divergent phenotype associated with two novel nonsense mutations in PRNP. Acta Neuropathol 2010;119:189-197.


·      Muñoz-Nieto M, Ramonet N,  López-Gastón NJI, et al. A novel mutation I215V in the PRNP gene associated with Creutzfeldt–Jakob and Alzheimer's diseases in three patients with divergent clinical phenotypes. J Neurol 2013;260:77-84.


Monday, February 1, 2016



 A 72-year-old patient went to a clinic complaining of weakness in his arms and legs, adding that he was tired at the end of the day. He had experienced a stroke two years earlier and recovered, but the CT scan and MRI of his brain showed no show signs of a repeat episode. So he was sent home.

    About two weeks later, the patient returned to the stroke clinic, this time seeing David Wang, DO, FAHA, FAAN, director of the Comprehensive Stroke Center at OSF Saint Francis Medical Center in Peoria, IL. The patient had the same complaints: weakness in his arms and legs and extreme fatigue at the end of the day.

     "These complaints sounded like a typical neuromuscular junction problem, so I started looking in a different direction, at myasthenia gravis," said Dr. Wang, a professor of neurology at the University of Illinois School of Medicine in Peoria.

        "The patient is now fine, and he's very appreciative," said Dr. Wang. He said the previous doctor misdiagnosed the condition because he was so focused on the stroke the patient had had two years earlier, and this was unrelated.



In an Institute of Medicine (IOM) report released in September, researchers declared diagnostic errors as the "blind spot" in health care, contributing to 10 percent of patient deaths and 6- to 17-percent of all hospital adverse events.

         Data from the Physician Insurers Association of America (PIAA), the insurance trade association representing medical professionals, suggest neurology is not immune. According, to the PIAA MPL Specialty Specific Series for Neurology 2014 Edition, diagnostic errors were the most prevalent factor in neurology claims and lawsuits, and were cited as the primary issue in nearly one-third of claims closed between 2009 and 2013. 

          Among those closed claims and lawsuits, approximately 32 percent resulted in an average indemnity payment of $539,598. Top patient outcomes related to diagnostic errors that resulted in an indemnity payment were occlusion of cerebral arteries; acute, but ill-defined cerebrovascular disease; and encephalopathy, according to the analysis.

         The IOM committee concluded that most people will experience one diagnostic error in their lifetime, but bemoaned the lack of data measuring diagnostic process and errors.

           To improve those numbers, the report suggested more of a teamwork approach to diagnosis, including more collaboration between health care professionals, providing patients with the tools to be more involved with the diagnostic process (such as, for example, finding errors in their electronic medical records), and encouraging more research.



Amar Dhand, MD, DPhil, an assistant professor of neurology at the Washington University School of Medicine in St. Louis, called the report "a landmark study."

   "It's a prevalent and serious problem. There aren't a lot of mechanisms to monitor the issue so we can sway the tide and stop it from happening," said Dr. Dhand, who coauthored an analysis of clinical decision-making among community-based neurologists in Neurology in 2013.   

     Dr. Dhand said part of the issue is that a misdiagnosis may play out over time; physicians often don't find out that they made an error because the patient has moved on.

     And one of the challenges with the teamwork approach is that not everyone is part of a larger group, he said. Private practitioners tend to be more solo artists, looking at neuroimaging and lab work and working off comments left in the electronic medical record (EMR).

      Academic groups have different problems.  It's more of a shared process of decision-making, but sometimes the work is left to trainees who do the initial intake and may miss something significant.

      "Because of the different social systems, each has different vulnerabilities," said Dr. Dhand. "The private practitioners are vulnerable because they may get into a routine or a habit of seeing things a certain way, and they are not as challenged by other neurologists.

      "In academia, you may not get all of the information. There's a detail voltage drop at every pass off, and the follow-up is distributed

across physicians so feedback of the end result doesn't make it to


        Dr. Wang, who co-chairs the AAN Quality and Safety Subcommittee, agreed that a lack of time with patients and the need to supervise interns and residents can contribute to more errors or misdiagnoses. He added that the overemphasis on imaging and not enough focus on a taking a detailed patient history and performing a physical, as well as doctor bias or stereotyping toward certain populations can also contribute to misdiagnoses.

"If a patient comes in and they are overweight [or they appear to have a drinking problem], the physician may just automatically blame the problem on their weight or their drinking. These patients may still have other neurological problems — a brain hemorrhage, for example, or an infection such as meningitis. If someone comes to the emergency department three or four times, they may be viewed as a repeater who is seeking attention, when they may possibly have other serious conditions such as a malignancy or stroke."

         EMRs help, but they also cause problems, he said. "We all see many patients a day, and the radiology report might be buried in the EMR and may not have been flagged. It's important for the radiologist to call the treating physician with the findings or diagnosis. This dialogue is very important in helping clinicians to make a correct diagnosis."

         At Washington University, he said, physicians created a diagnostic monitoring tool where neurologists must outline the process used to make a diagnosis, from physical exam and patient history to lab work and scans.

Eric Cheng, MD, FAAN, the interim chief medical informatics officer and an associate professor at the David Geffen School of Medicine at the University of California, Los Angeles, said it is very difficult to develop quantifiable quality measures regarding a diagnosis, because symptoms are not recorded as discrete data. For example, "difficulty walking" may be a symptom of Parkinson's disease, but it is not specific enough. It would not be appropriate to ask physicians to document why every patient with difficulty walking does or does not have the diagnosis of Parkinson's disease, he said.

           While electronic health records make it easier to propagate information, they also make it harder to correct misinformation. 

"Once a physician records a diagnosis, it can become really, really hard to reverse it. Let's say PCP A makes an incorrect diagnosis. Specialist B copies that diagnosis into a note. Specialist C (let's assume this is the neurologist) makes the correct diagnosis.  PCP A reads the neurologist's note and does the right thing in correcting the diagnosis in his or her note," Dr. Cheng said.  "But if specialist B copies forward his or her own previous note with the wrong diagnosis, it still remains [in the record]."

"As part of a grant sponsored by a disease specialty society, I interviewed patients about their care," Dr. Cheng said. "I thought they would most want to discuss their quality of care or access to specialists. I was surprised that quite a few patients wanted to express their anger about being initially misdiagnosed. Even if they believed they were currently receiving good care, they still harbored mistrust of the health care system because of those early experiences."


  • ​The Institute of Medicine Report, "Improving Diagnosis in Healthcare":

Wednesday, January 27, 2016


Public health officials in the United States are gearing up surveillance efforts following reports that potentially link the Zika virus to an increased risk of Guillain–Barré syndrome (GBS) and microcephaly in fetuses and newborns.

Zika, a mosquito-borne virus, has been tracked to 21 countries and territories in South America, Central America, and the Caribbean, mostly in the last two months. At press time, two cases of Zika virus were detected in the US Virgin Islands and Puerto Rico.

The Centers for Disease Control and Prevention (CDC) has issued a travel advisory, warning pregnant women to avoid travel to these regions, and has asked health care professionals and state and local public health departments to report flu like-symptoms or GBS in patients (including pregnant women) who have traveled to and from the countries affected.

The "unusual and unexpected neurological manifestations are very troubling," James Sejvar, MD, a neurologist and epidemiologist at the CDC, told Neurology Today. "We are working hard to understand the virus and prevent its spread."

Dr. Sejvar is now in Brazil heading a team studying the epidemic to learn more about how the virus is associated with GBS and microcephaly.

At press time, the Zika virus had been detected in one person in Puerto Rico without a history of travel, and an infant in Hawaii born with microcephaly had evidence of Zika infection. According to public health officials, the mother was living in Brazil while pregnant.

Eighty percent of people infected with the Zika virus remain asymptomatic and 20 percent develop a mild flu-like illness that can last a week and include fever, rash, joint pain, and conjunctivitis. It is not yet known how often someone infected with the virus will go on to develop GBS; nor is the risk known for microcephaly in babies born to women exposed in pregnancy.

Daniel Pastula, MD, MHS, a neurologist and medical epidemiologist at the University of Colorado School of Medicine, told Neurology Today that Zika virus is transmitted from certain Aedes species of mosquitoes to humans. If an infected person gets bit by another Aedes mosquito, then that mosquito becomes infected and can spread the virus to other humans, creating a human-mosquito-human transmission cycle.

There are no current disease-modifying treatments or vaccines against Zika virus disease, he noted, adding that prevention is key. People can avoid mosquito bites "by wearing long sleeved-shirts and pants when feasible, applying insect repellent when outdoors, and using window screens and air conditioning when indoors," he said.

So far, outside of Puerto Rico, there are no reports of local Zika virus transmission on American soil. But it is only a matter of time before new areas are affected, experts agree. And the neurological signs have health officials worried.



Beginning in 2013, Zika virus disease started spreading throughout islands of the Pacific Ocean, affecting residents French Polynesia. Epidemiological evidence suggested that tens of thousands of people, or 10 percent of its inhabitants, were exposed to the virus. Those who got sick had only mild flu-like symptoms. But a few weeks after the symptoms subsided, medical centers began seeing a growing number of people presenting with GBS.

"It was magnitudes higher than normal," Dr. Sejvar said.  The island had another outbreak in 2014. Again, GBS escalated. Three thousand miles away, cases were detected in New Caledonia, and that same year, another GBS cluster was reported in Fiji.

Dr. Sejvar led a team that traveled to Fiji in 2014 but by the time they arrived it was not possible to definitively detect the virus in the serum of the patients who went on to develop GBS. Fiji was in the throes of a large dengue epidemic, which made interpretation of serologic results challenging because of cross-reactivity between the flaviviruses. From February to May, the island country had nine documented cases of GBS, which was up to five times the expected number.

By May 2015, local transmission of Zika virus was first reported in Brazil. Dr. Sejvar said that it is not clear how the virus arrived in Brazil; some hypothesize that Zika virus could have been carried into the country through someone who traveled there for the World Cup in June 2014. Hundreds of thousands of people, maybe millions, were infected with the Zika virus, he said. About 30,000 people developed mild flu-like symptoms. The peak of the infectivity may have been in the summer of 2015, he said, pointing out that around that time clinicians in northern Brazil started reporting higher than normal rates of GBS.

The CDC immediately launched a co-investigation with the Brazil Ministry of Health. In November, Dr. Sejvar arrived for initial discussions with the Ministry to review their data and assess the situation.  During these meetings, the Ministry demonstrated there was an approximate two to three week lag between the peak of reported Zika cases and the development of GBS.

"It was very convincing," said Dr. Sejvar. "At that time the country had PCR testing, which detects Zika-specific RNA during the early stages of illness.  However, by the time a person develops GBS signs, it is too late to find viral RNA in biological specimens from patients."

Dr. Sejvar completed his assessment and flew back to the US. Dr. Sejvar recommended to the Brazilian Ministry of Health that CDC epidemiologists return to conduct a case-control serological study; that study began last month.

There are 45 reported GBS cases in the state of Bahia in northern Brazil. Dr. Sejvar and his team are taking blood samples from these patients and an equal number of age-matched controls to conduct antibody tests for an immunoglobulin-G (IgG) response to the virus. These tests will be done at CDC facilities in Fort Collins, CO, and Atlanta.

"Given the fact that Brazil has only seen the Zika virus for one year, the IgG response should be a good indication of infectivity and tell us whether they had been exposed to Zika, though there are concerns about cross-reactivity of these antibodies to dengue," Dr. Sejvar said. The team will also test to determine whether the sera from people who developed GBS neutralizes or kills the Zika virus in culture.

A separate team from the United States is traveling to train local health practitioners to conduct serological testing in Brazil.

El Salvador also reported 46 cases of GBS in a one-month period from December to early January, Dr. Sejvar said. Two of these patients died. Normally, the country sees four cases a month. CDC epidemiologists were able to look at medical information on 22 of these patients and half of them had reported a fever and rash a few weeks before the onset of GBS.

Dr. Sejvar stressed that there are temporal and spatial links between the virus and GBS. A direct link is still being investigated. In French Polynesia, there were reports of other neurological conditions — meningitis, meningoencephalitis, and myelitis — in addition to GBS.  



It is not known whether Zika virus is directly responsible for microcephaly, but there is increasing evidence of a possible association. As of January, there have been as many as 3,893 women in Brazil who gave birth to a child with microcephaly. The government began testing for Zika infections in the mothers and found a high number of them reported being ill with the classic fever and rash during the pregnancy. The country usually documents, on average, 163 cases a year. Tissue from two fetuses lost during the pregnancy and two newborns who died within the first day of life tested positive for the Zika virus. All four had smaller than normal brains.

Local Brazilian scientists also found Zika virus in the amniotic fluid of two pregnant women and in the placenta of another woman who miscarried. The CDC is now seeking approvals from the Brazilian Ministry of Health to conduct a case control study to see if they can link the two conditions and learn more about how the virus might be causing birth defects.

The fetal and newborn tissue that was studied showed damage to the developing brain, Cynthia Moore, MD, PhD, director of the CDC's division of birth defects and developmental disabilities, said at a press briefing in mid-January.

 "It's very hard to say how much of an increase it [microcephaly] is," she said. "We're also seeing babies who have severe microcephaly, much more than we would expect."

 It seems that the mother's exposure [to Zika] was often during the first and second trimester, although studies are still underway, Dr. Moore said.

Lyle Petersen, MD, MPH, director of the division of vector-borne diseases in the National Center for Emerging and Zoonotic Infectious Diseases, added at the briefing: "I think we're just going to have to wait to see how this all plays out. These viruses certainly can spread in populations for some time. But, again, this is new. I think it's really impossible for us to speculate what may happen in three or four (weeks) or even next month for that matter."

J. David Beckham, MD, an associate professor at University of Colorado School of Medicine's division of infectious diseases, studies the pathogenesis of viral infections in the central nervous system, and is getting the proper regulatory approvals to begin testing Zika virus. His lab has focused on West Nile and other flaviviruses. When the Zika virus first emerged, Dr. Beckham contacted Aaron Brault, PhD, a virologist at the CDC, to collaborate on developing a model system for how the vector moves from source to source, and then study how it affects neurons. Dr. Beckham and his colleagues developed a laboratory model of the West Nile virus and he is hoping to do the same with the Zika virus.

"There are a lot of unanswered questions," said Dr. Beckham. "Right now, there is an epidemiological association. This has everyone in our field very concerned."






  • Staples JE, Dziuban EJ, Fischer M, et al. Interim guidelines for the evaluation and testing of infants with possible congenital Zika virus infection — United States, 2016. MMWR Morb Mortal Wkly Rep 2016;65(Early Release):1–5; Epub 2016 Jan. 26.


  • Epidemiological update: neurological syndrome, congenital abnormalities, and Zika virus infection. Pan American Health Organization and World Health Organization. January 17, 2016.


  • Musso D, Nilles EJ, Cao-Lormeau. Rapid spread of emerging Zika in the Pacific area. Clin Microbiol and Infect 2014; 20(10);O595-596.


  • Duffy MR, Chen T-H, Hancock T, et al.  Zika virus outbreak on Yap island, Federated States of Micronesia. N Engl J Med 2009, 360:2536-2543.


  • Oehler E, Watrin L, Larre P,  et al. Zika virus infection complicated by Guillain-Barre syndrome – case report, French Polynesia, December 2013. Euro Surveill 2014; 19(9). pii:20720.​