Listing of Nerve Disorders Associated with Zika Grows


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Neurological and Neuromuscular Diseases: Mayo Clinic Radio

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WEDNESDAY, March 9, 2016 (HealthDay News) The list of neurological disorders potentially associated with the Zika virus continues to grow, health officials reported Wednesday. Writing in the March 9 online edition of the New England Journal of Medicine, French researchers described the case of an. Another Neurological Disorder Tied to Zika. It may cause meningoencephalitis, an infection and swelling of the brain, researchers say.

The list of neurological disorders potentially associated with the Zika virus continues to grow, according to a letter to the editor and a perspective piece published online in the New England. Another neurological disorder tied to Zika Researchers warn it may also cause meningoencephalitis, an infection and swelling of the brain. By: Dennis Thompson More articles by Dennis Thompson. WEDNESDAY, March 9, 2016 The list of neurological disorders potentially associated with the Zika virus continues to grow, health officials reported Wednesday.. Writing in the Wednesday online.

By Dennis Thompson HealthDay Reporter. WEDNESDAY, March 9, 2016 (HealthDay News) The list of neurological disorders potentially associated with the Zika virus continues to grow, health officials reported Wednesday.. Writing in the March 9 online edition of the New England Journal of Medicine, French researchers described the case of an unidentified 81-year-old man who had. NEURO-ZIKA: Neurological Manifestations of Zika Guillain-Barré syndrome is a major complication of Zika virus and occurs in 1 in 4,000 or 5,000 cases, which makes it potentially a huge burden to healthcare providers and systems. Central nervous system disease is.

List of Possible Zika Birth Defects Grows Longer Even without microcephaly, seizures and developmental delays may appear in the months following birth By. MONDAY, Aug. 14, 2017 (HealthDay News) Adults infected with the Zika virus can develop a number of serious neurological conditions, a new study finds.

Until now, the most troubling Zika-related. Congenital Zika virus infection has also been associated with other abnormalities, including but not limited to brain atrophy and asymmetry, abnormally formed or absent brain structures, hydrocephalus, and neuronal migration disorders. Other anomalies include excessive and redundant scalp skin.

List of related literature:

There is also concern that Zika virus infection may be associated with the development of Guillain-Barré syndrome (Chapter 39: Viral Syndromes).

“Fenner and White's Medical Virology” by Christopher J. Burrell, Colin R. Howard, Frederick A. Murphy
from Fenner and White’s Medical Virology
by Christopher J. Burrell, Colin R. Howard, Frederick A. Murphy
Elsevier Science, 2016

Other problems have been detected among fetuses and infants infected with Zika virus before birth, such as absent or poorly developed brain structures, defects of the eye, hearing deficits, and impaired growth.

“Modern Dental Assisting E-Book” by Doni L. Bird, Debbie S. Robinson
from Modern Dental Assisting E-Book
by Doni L. Bird, Debbie S. Robinson
Elsevier Health Sciences, 2020

• Congenital Zika syndrome now described, including cognitive, motor, and sensory disabilities plus: • Severe microcephaly with partial collapse of skull (Fig.

“Comprehensive Review of Infectious Diseases” by Andrej Spec, Gerome V. Escota, Courtney Chrisler, Bethany Davies
from Comprehensive Review of Infectious Diseases
by Andrej Spec, Gerome V. Escota, et. al.
Elsevier Health Sciences, 2019

Zika virus infection may also trigger a range of neurological complications ranging from Guillain-Barré syndrome, neuropathytomyelitis, particularly in adults and older children.

“IAPSM's Textbook of Community Medicine” by AM Kadri
from IAPSM’s Textbook of Community Medicine
by AM Kadri
Jaypee Brothers,Medical Publishers Pvt. Limited, 2019

Most Zika virus infections are asymptomatic, but congenital Zika virus has caused fetal loss as well as microcephaly and other serious neurologic anomalies (AAP, 2018f).

“Breastfeeding and Human Lactation” by Karen Wambach, Becky Spencer
from Breastfeeding and Human Lactation
by Karen Wambach, Becky Spencer
Jones & Bartlett Learning, 2019

Vertical transmission of the virus leads to congenital Zika virus infection; sequelae include microcephaly with brain anomalies (and other serious neurologic consequences) and fetal loss.

“CDC Yellow Book 2020: Health Information for International Travel” by CENTERS FOR DISEASE CONTROL AND PREVENTION. (CDC), Gary W. Brunette
from CDC Yellow Book 2020: Health Information for International Travel
OXFORD University Press, 2019

Zika virus infection as a cause of congenital brain abnormalities and Guillain-Barre syndrome: systematic review.

“Creasy and Resnik's Maternal-Fetal Medicine: Principles and Practice E-Book” by Robert Resnik, Charles J. Lockwood, Thomas Moore, Michael F Greene, Joshua Copel, Robert M Silver
from Creasy and Resnik’s Maternal-Fetal Medicine: Principles and Practice E-Book
by Robert Resnik, Charles J. Lockwood, et. al.
Elsevier Health Sciences, 2018

Zika infection during pregnancy may cause severe birth defects including microcephaly and fetal death, and patients have developed Guillain–Barré syndrome.

“Habif' Clinical Dermatology E-Book” by James G. H. Dinulos
from Habif’ Clinical Dermatology E-Book
by James G. H. Dinulos
Elsevier Health Sciences, 2019

The dark side of Zika infections include two other syndromes: microcephaly and Guillain-Barré Syndrome (GBS).

“Microbiology: Principles and Explorations” by Jacquelyn G. Black, Laura J. Black
from Microbiology: Principles and Explorations
by Jacquelyn G. Black, Laura J. Black
Wiley, 2018

Other ocular findings include optic nerve hypoplasia, severe optic disc cupping, lens subluxation, and iris colobomas.77 A widespread outbreak of Zika virus began in April 2015 in Brazil, and has spread to other countries in South America, Central America, Mexico and the Caribbean.

“Taylor and Hoyt's Pediatric Ophthalmology and Strabismus E-Book” by Christopher J. Lyons, Scott R. Lambert
from Taylor and Hoyt’s Pediatric Ophthalmology and Strabismus E-Book
by Christopher J. Lyons, Scott R. Lambert
Elsevier Health Sciences, 2016

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  • The medical establishment has spun me around in circles, with lots of tests, radiology, with no cause, disorder, or disease, therefore no treatment… how soon will this turn into, if it’s not already “cancer?”… I’m slipping through the cracks, and I feel like I’m not going to be with us too much longer.

  • It took ten years to diagnose me with FND and I know exactly when it started. I had just got married, we where crazy in love and I was at the happiest point in my life… then it struck. Doctors like to insist that there has to be some sort of underlying stress, a virus or something at least with the onset and that simply isn’t true. Stress and other illnesses contributes to it just like they contributes to any physical illness but I don’t believe for a moment that stress is the cause.

  • Hi my name is Riaz Ahmed & I m from Balochistan want ur help in case of my nephew age 11 years who have brain gene problem having problem in walking and coordination issue, diagnosed by local doctors and they said that there is no any medical treatment for such neurological disease and its neurological problem in brain due to genes….i have the medical reports of child and M.R.I scan CD also availble if desire….hope for ur answer if any treatment available in world for such patients…

    Riaz Ahmed

  • It is important to note that FND is not necessarily a psychological condition. There can also be a physiological cause. Mine were caused by an adverse reaction to medication. I have met others with a brain injury and another with pancreas disfunction whose injuries have caused non-epileptic in my small town, also not psychologically induced.
    “Older ideas that FND is “all psychological” and that the diagnosis is made only when someone has normal tests have changed since the mid-2000s. The new understanding, including modern neuroscientific studies, has shown that FND is not a diagnosis of exclusion. It has specific clinical features of its own and is a disorder of the nervous system functioning in which many perspectives are necessary. These vary a lot from person to person. In some people, psychological factors are important, in others they are not.”
    … “In some psychological factors such as past trauma or stress at the time of symptom onset in FND are important in understanding how the brain has gone wrong. In others the presence of a problem like migraine or a physical injury may be the most important thing.”
    From the National Organization for Rare Diseases (NORD) website.

  • Sir, I have 14days baby, preterm delivery in 35week. Done USG Skull today and mentioned in report There is a heterogeneous elongated oval lesion centered in right lateral ventricle at posterior horn, in the region of choroid plexus. It extends into frontal and occipital horns of lateral ventricle as well. It has a hyperechoic rim with central heterogeneous echogenicity. There is periventricular hyperechogenetic on the right side. Kindly suggest us according to the report.

  • Recovery is not possible for everyone. I have a dead spot in my brain that is causing this. Unfortunately that doesn’t stop the knee jerk reaction of the very few people who know about the disorder because they will still tell you the cure is to accept that it is not really happening. I was told that to get past this I have to ignore the events. This is grossly negligent and dismissive. Have you ever tried ignoring dystonia? What about spinal myoclonus… how easy is that to ignore? Drop foot and loss of sensation of outer extremities. Can you ignore that? The truth is, medical science has very little information about this and has spent hundreds of years pretending it wasn’t even a real disorder. That’s why they had to change the name of it.

    “It is a capital mistake to theorize before one has data. Insensibly one begins to twist facts to suit theories, instead of theories to suit facts.” Arthur Conan Doyle

  • I am the 2nd oldest person out of 110 in the whole world with Abetalipoproteinemia check out my videos and google search on my name thank you

  • Reptilian brain….. hhhmmmm makes me now believe certain people are reptilian! Like you see here in YouTube look it up lol wow I cant believe this doctor just said that!!!

  • A very informative video. But there’s a significant problem with FND that is ignored in this video. The video acknowledges that approximately 37 percent of FND cases can be caused by an injury. Yet, since FND is listed in the DSM 5, various clinicians and others automatically list FND as a Pysychological condition. As a result those patients are denied the proper “Physical” treatments that they need in order to recover. How many FND sufferers are out there that could have recovered correctly had their condition not been listed as a Psychological condition?

  • I was given Norflex injection when I went to the hospital. I had no problems with my nerves I only went to the hospital because I thought I had a UTI or kidney problem the nurse asked how I felt I said I was experiencing alot of pain mostly in my back where the kidneys are. He came in and place an IV in arm and injected me with Norflex a muscle relaxer I was about to die my head felt like it was burning my body couldn’t move, my blood pressure was 289/173. Now every day I feel faint I keep having tingling feeling in my legs and arms. I feel like my head is burning. I don’t know what to do. Please hep

  • My husband has something that we haven’t been able to figure out. It happens mostly when he’s asleep or exhausted. Moments later he wont be able to move. He can faintly speak out to me saying “help!”. His body is paralyzed and I have to physically get on top of him and grab behold his neck in order to pull him up and he regains movements. He’ll be extremely tired afterwards or have migraines. It can happen back to back and we are clueless on what kind help he may need. They are seizure-like but not seizures. It has to be surgical.

  • Great harm is done by patients with ME/CFS when wrongly diagnosed as FND. When the chronic, multisystem, autoimmune disorder, ME/CFS, is misdiagnosed as being a psychiatric complaint, patients are offered CBT, which is irrelevant to a non-psychiatric illness, and GET, Graded Exercise Therapy, which in many cases pushes a mildly or moderately ill patient into permanent and complete incapacity and intractable pain. The Institute of Medicine (Now the Academy of Medicine) commissioned a report on ME/CFS which was published in February, 2015. The core finding of this Commission was that this is a non-psychogenic multisystem very disabling disease. It’s defining aspect is that exertion, of any type, physical, cognitive or emotional, ‘may adversely affect many organ systems’. Most usually precipitated by an apparently mild virus, from which the patient does not recover, the most appropriate first response to this symptom pattern is to advise an extended period of complete rest, thus conserving the patient’s energy for the use of the immune system. Before this illness was taken over by psychiatry, a significant proportion of patients recovered completely, or virtually completely. The current treatments have resulted in a situation in which almost no one recovers, and the illness has come to be regarded as one of almost inevitable consistent deterioration.
    Typically ME/CFS patients are high-functioning, conscientious individuals, very often in physically demanding professions: athletes, dancers, marathonners, back=packers, or manual workers, or nurses, carers for disabled or elderly family members, mothers of young children.
    If you have been diagnosed with FND, but know that your illness followed a viral illness, in the context of a generally happy and successful life, and you know that you are not suffering from anxiety or depression (except because your illness has completely disrupted your life), you do not have FND. You need to conserve exertion, and avoid any suggestion that you should ‘push through’. If your medical advisors tell you otherwise, their advice, however well-meant, is a danger to you. Find out about ME/CFS and make your decisions accordingly.

  • My daughter was recently diagnoses with FND. I wish I would have found this video sooner as it has been a world of help to me. I have shared it with some family members and asked them to watch it as well. I feel much better about her diagnosis and how we can handle it now that I have seen this. THANK YOU!


    Neuroblasts generated in the subgranular zone did not migrate to the hippocampal CA regions, and thus the new neurons found in the injured the site may be derived from the SVZ (Ruan et al., 2014). There are studies reporting a twoto fourfold increase of neuroblasts after TBI (Lu et al., 2003; Ramaswamy et al., 2005), which is comparable to the increase in the SVZ. The cortex is another site where the activated neural precursor cells could be found after TBI. Magavi, Leavitt, & Macklis (2000) found that after neuronal death, the dormant NPCs in the cortex activate and differentiate into mature neurons and establish synaptic connections in the adult rodent. The nestin, a marker of neural stem cells, is found in the peri-injured cortex 7days post-injury, suggesting the possibility of NPC activation (Kernie, Erwin, & Parada, 2001). In animals of the controlled cortical impact model, when the cortical tissue was isolated, nestin expression peaks in vitro 3days after injury, and is associated with the formation of neurospheres (Itoh, Satou, Hashimoto, & Ito, 2005). The capacity of human cortical NPCs to generate new neurons was also found after TBI (Arsenijevic et al., 2001; Richardson, Holloway, Bullock, Broaddus, & Fillmore, 2006), which suggests that the cortical dormant NPCs are a possible source of new neurons after injury. Animal studies showing improvement in functional outcome by augmenting neurogenesis following TBI have suggested the functional role of newborn neurons in this injury. In a physiological condition, neural progenitors in the SVZ migrate to the olfactory bulb and differentiate into inhibitory interneurons or dopaminergic periglomerular neurons (Ruan et al., 2014). These progenitors of the SVZ can differentiate into calbindin expressing neurons when they are engrafted into the DG (Richardson et al., 2005). Exogenously transplanted neural precursor cells in the TBI animal Conclusions 265 brains can differentiate into mature neurons and promote functional and cognitive outcomes (Blaya, Tsoulfas, Bramlett, & Dietrich, 2015). Furthermore, treatment of TBI animals with pro neurogenic medications such as statins, erythropoietin, and fibroblast growth factor 2 enhances neurogenesis in the SVZ and promotes functional outcomes (Lu et al., 2005, 2007; Sun et al., 2009; Xie et al., 2014). In contrast, inhibition of the injury-induced

    neurogenesis suppresses cognitive recovery in TBI models (Sun, Daniels, Rofle, Waters, & Hamm, 2014). From the above-noted findings, it is known those new neurons could potentially develop into mature and functional neurons in the proper niche. The neurons may integrate into the existing neural circuit directly or benefit by secreting neurotrophic factors to promote the survival and functioning of the affected neurons. Since both TBI and stroke are associated with promoted endogenous neurogenesis that may benefit rehabilitation, understanding the underlying mechanisms can be beneficial to the treatment regimen of both diseases.


    Despite that the significance of adult neurogenesis in pathological
    conditions have been investigated for decades, its role in the etiology and therapeutic treatments are still under investigation. Evidence from both preclinical and clinical studies support the hypothesis that neurogenesis participates in disease conditions in the CNS. Different aspects of neurogenesis have been intensively investigated, for instance, the behavioral/physiological significance of neurogenesis, the regulatory mechanisms of the neurogenesis process, modalities that regulate neurogenesis, roles of neurogenesis in neurological diseases and recovery, and potential application of pro neurogenic treatment in human studies. In general, alternations

    in adult, neurogenesis has been suggested to be related to neurological disorders, while treatments which could modulate neurogenesis are hoped to be the future treatments. Preclinical studies would provide valuable information for understanding the process of adult neurogenesis, the efficacy of pro neurogenic treatment on the aforementioned diseases, and

    the mechanisms underlying the pathology. For the potential translation of the
    knowledge obtained from animal studies, clinical studies would need to reveal more about changes and functions of adult neurogenesis in neurological disorders. While both preclinical and clinical studies are crucial for the final application of treatment and understanding of CNS diseases, the translation of knowledge from basic science to clinical studies will be a great challenge. Promoting collaboration between both parties would greatly facilitate the development of effective treatment for neurogenesis-related brain disorders.

  • This was horrible, it’s not always triggered by stressful event, they don’t explain that the brain does not communicate well with the body, there is something with the brains signaling. It’s not a fascinating story it’s frightening, you go looking for help cause u can barely function and no one can help you

  • I was diagnosed with FND 2.5 years ago after I ruptured my L4/L5 disc, it presented as almost complete paralysis and loss of sensation below the knee of my right leg. I now walk with a cane and an AFO brace but have shown no other signs of recovery, nothing seems to have any effect and to hear someone describe this condition as “fun” is actually pretty insulting.