Guillain-Barré Syndrome

Guillain-Barré Syndrome: Survivors Share Experience

Guillain-Barré Syndrome | Johns Hopkins Medicine

Kim Earnshaw was 18 years old when she woke one morning and noticed she couldn’t feel the tips of her middle fingers.

The next day her feet felt funny.

The day after, she told her parents about the lack of sensation in her hands and feet and saw a doctor.

The doctor chalked it up to a protein deficiency and sent her home, but by the next morning the numbness had traveled.

“I couldn’t feel my feet,” Earnshaw told Healthline. “I put my feet down on the hardwood floor and it hurt.”

Earnshaw ignored the numbness. She went to her job at a seafood counter in a local grocery store.

That night she was doing inventory at the counter. She had to weigh 20-pound boxes of seafood and log the information into a spreadsheet. Within 20 minutes Earnshaw could no longer lift the boxes or even read the numbers on the spreadsheet.

Scared, she sprinted to the front of the store.

“I was running down the aisle and kept falling and falling,” she said.

That evening Earnshaw was diagnosed with Guillain-Barré syndrome (GBS). Her paralysis lasted almost two months.

Read More: Get the Facts on Guillain-Barr »

Nervous System Assault

GBS is an autoimmune disorder that attacks the body’s peripheral nervous system and causes paralysis, according to the National Institute of Neurological Disorders and Stroke.

Symptoms usually start at the feet and work their way up the body. GBS can also affect organs, forcing some patients to receive a tracheotomy to breathe.

It’s estimated that roughly one in 100,000 people will develop GBS.

While researchers are unclear why some people develop the disorder, they agree it’s triggered by a bacterial or viral infection.

“There is definitely tight epidemiology between campylobacter bacteria and Guillain-Barré syndrome,” said Dr. Michael Wilson, assistant professor of neurology at the University of California San Francisco (UCSF) School of Medicine.

More recently the Centers for Disease Control and Prevention (CDC) declared that there is a correlation between GBS and the Zika virus.

A number of Latin American countries have reported high rates of GBS during the Zika outbreak. Brazilian cases of GBS jumped 19 percent between 2014 and 2015. El Salvador saw 104 cases of GBS in one month during a Zika outbreak last year, compared to a yearly average of about 170 cases.

French Polynesia had a Zika outbreak from October 2013 to April 2014 and saw roughly 40 cases of GBS during that same time. Plotted on a chart, Wilson said the timeline reveals an increase in GBS as Zika starts to wind down. The lag time is considered textbook when looking at how outbreaks manifest, he noted.

There are two hypotheses around the connections between the virus and GBS, according to Wilson. Either Zika has caused GBS for decades and people didn’t notice, or the virus has mutated.

“The jury is still out,” he said.

Read More: Dengue Vaccine Could Pave the Way for Zika Vaccine »

Swift Moving Disease

Regardless of how someone gets GBS, the onset of symptoms is swift.

Earnshaw was completely paralyzed within 10 days.

For Cindy Conklin Hughes, her paralysis caused by GBS came on in about half that time.

Conklin Hughes was almost 21 years old when she noticed something was off while driving home from a new job. She couldn’t feel the brake pedals. The next morning her legs felt weak and her breakfast tasted tinfoil.

Just seven days from that initial onset, Conklin Hughes found herself at UCSF Benioff Children’s Hospital where she’d received a tracheotomy to help her breath.

“I couldn’t talk, I had double vision,” Conklin Hughes told Healthline. “No function, no control. I needed diapers. It was horrific, and it was that for a month.”

Since developing GBS nearly 30 years ago both women have gone on to live normal lives.

Today, Conklin Hughes, 50, is married with three children. Earnshaw, 48, is also married, and has two children.

Still, the memories surrounding their bouts with GBS remain vivid. Both can recall in great detail what it was to be paralyzed.

“People would tell me to close my eyes and would be poking me and I couldn’t really feel it,” Hughes said. “But then they would rub me and it would hurt so bad.”

Earnshaw said it was almost an out-of-body experience.

“It felt I didn’t know where my extremities were,” she said. “I’d get these pains, but I didn’t know where they were coming from.”

Read More: Scientists Unlocking the Mystery of How Our Immune System Works »

Origin Still Unknown

Hughes said her doctors never pinpointed how she developed GBS.

Earnshaw’s doctors suspected she was exposed to the campylobacter bacteria because of her job. The meat department in the grocery store was right next to the seafood counter, so that theory made sense.

While the cause of GBS is unclear, scientists do know what happens in the body when it occurs.

The body’s immune system starts to destroy the myelin sheaths that surround peripheral nerves. These nerves control body function and when the sheaths are damaged nerves can’t communicate with the brain.

“So the damage from Guillain-Barré can be motor problems, sensory problems, or both,” said Dr. Carlos A. Pardo-Villamizar, an associate professor of neurology and pathology at Johns Hopkins University.

There are two types of treatments to combat GBS. The most common today is intravenous immunoglobulin treatment (IVIG). Patients receive an infusion of immunoglobulin extracted from the plasma of donated blood.

The other treatment is plasmapheresis. Also called plasma exchange, the process is similar to dialysis. A person’s blood is withdrawn, the “bad” plasma is replaced with “good” plasma, and then the blood is pumped back into the patient.

Earnshaw and Hughes both went through plasmapheresis, which they say was extremely painful and took hours at a time to complete. However, they credit the treatment with their recovery.

“All of a sudden, I could move my hands,” Earnshaw said.

Read More: E. Coli and Salmonella Infections Are Down, but Other Foodborne Illnesses Are Up »

No Easy Road to Recovery

The recovery, though, was short-lived. Both women experienced setbacks.

Conklin Hughes had transferred to a rehabilitation center, only to be sent back to the UCSF children’s medical facility. The move back to the hospital was devastating.

“You just question why, why, why,” Conklin Hughes said. “You ask yourself, ‘Am I ever going to walk again?’”

Earnshaw said she started to feel hopeless when it became clear that her recovery had plateaued.

“I panicked and freaked out,” she said, tearing up as she remembered the experience. “I was so upset and crying. I didn’t think I was going to make it.”

After another set of plasmapheresis treatments both women found themselves in recovery and for good this time. The numbness eventually disappeared.

Soon Earnshaw could sit up by herself. Conklin Hughes didn’t need a machine to help her breath. They still both had muscle weakness and needed wheelchairs and walkers.

Conklin Hughes entered rehab again to get her strength back. It took a year before she felt her old self.

“I had to learn everything all over again,” she said. “Walking, talking, fine motor skills, everything.”

Earnshaw ended up rehabbing at home because of an employee strike at the center she was supposed to enter. She said it took about four months to recover.

Read More: Cancer Treatment Leaves Survivors with PTSD Scars »

Lingering Effects

The difference in recovery time between the two women is common, Pardo-Villamizar said. That’s because IVIG and plasmapheresis treatments don’t technically “cure” patients with GBS.

“They help to control the response [of the disorder], but it’s not going to help in the remylination of peripheral nerves,” he said. “That result is [done] by the patient’s own body.”

Most people with GBS make a full recovery. Just 5 percent of patients see a recurrence.

In general, the long-term effects are mild. Earnshaw’s fingers get numb when exposed to snow or icy conditions, and Conklin Hughes’ feet get numb in a matter of minutes when exposed to cold.

Aside from the physical issues, both women said GBS took an emotional toll. Still, Conklin Hughes was determined to fight GBS and walk again.

“I never once gave up,” she said.

Earnshaw said once she recovered, she didn’t look back on her experience for years, but today is retrospective about what she went through.

“Once I was done with it, I was done,” she said. “I wanted to live life to the fullest.”

Source: https://www.healthline.com/health-news/surviving-guillain-barre-syndrome

Guillain-Barré Syndrome | Johns Hopkins Medicine

In a collaborative effort with scientists at six Colombian hospitals, Johns Hopkins Medicine researchers report what they believe to be the strongest biological evidence to date linking Zika virus infection and Guillain-Barré syndrome.

Epidemiology data have long suggested a close relationship between rising Zika virus infection rates and instances of Guillain-Barré. The new study's results, published on Oct. 5 in The New England Journal of Medicine, support the correlation with immunologic and viral evidence of Zika infection in a substantial number of people with Guillain-Barré, the investigators say.

Guillain-Barré is a very rare but potentially paralyzing disorder of the nervous system that appears days to weeks after infection with viruses or bacteria.

A so-called post-infectious immune condition, it occurs when a person's own immune system attacks the myelin sheaths that protect the body's nerve cells, often resulting in muscle weakness, pain, sensory deficiencies and, in very acute cases, paralysis.

Guillain-Barré, which affects an estimated one or two 100,000 people after infections, is diagnosed with electrodiagnostic neurological tests that measure the conductive speed and activity of nerve signals. Scientists do not know why it strikes some people and not others.

“At the beginning of the Zika outbreak in South America, my colleagues in Colombia contacted me with concern about the increasing number of patients with neurological complications in their hospitals,” says Carlos A. Pardo, M.D.

, associate professor of neurology and pathology at the Johns Hopkins University School of Medicine, who earned his medical degree in Colombia and is an expert in neuroimmune and infectious diseases, including Guillain-Barré.

For the new study, Pardo's team designed strategies with colleagues in Colombia to evaluate patients with suspected neurological problems associated with Zika and provided tools for viral tests of blood, cerebrospinal fluid and urine samples from 68 people with symptoms of Guillain-Barré. Of the 68 patients initially evaluated in Colombia, virus and immunology studies were conducted using the body fluids from 42. After some evaluation, the researchers found urine to be the most reliable fluid to diagnose Zika infection in patients with Guillain-Barré.

Seventeen patients tested positive for Zika virus in their urine.

Another 18 had no evidence of Zika virus in urine but showed the immunologic footprints of Zika infection through the presence of virus-specific antibodies in their blood or spinal fluid.

Most of the patients were adults — 38 were males, and 30 were females of an average of 47 years old. Almost all patients displayed two or more clinical symptoms of Zika infection, which include fever, headache, rash and conjunctivitis.

The researchers say that almost one-half of the study participants complained of neurologic symptoms within four days of the onset of Zika symptoms — an unusually fast response, they say, than is found in people who develop Guillain-Barré symptoms after other viral infections, such as influenza and herpesviruses.

Tests also revealed that most of the 46 patients whose Guillain-Barré was confirmed by electrodiagnostic neurological tests had the acute inflammatory demyelinating polyneuropathy variant of the disorder. This type of Guillain-Barré attacks the myelin, a protective group of cells that insulates the surface of the nerve fibers, the plastic coating on a copper wire.

Pardo says the study is believed to be the largest of its kind to document the role of Zika infection in increased rates of Guillain-Barré so far. But he cautions that although the study demonstrates a biological and viral association between Zika infection and Guillain-Barré, it does not reveal the biological mechanisms through which Zika might initiate an immune attack on the nerves.

The research team, he says, continues to collect clinical data and samples from the Colombian hospitals' patients, but the work is constrained by the limited availability of resources, which is further strained by the severe and ongoing Zika outbreak in South America.

Story Source:

Materials provided by Johns Hopkins Medicine. Note: Content may be edited for style and length.

Journal Reference:

  1. Beatriz Parra, Jairo Lizarazo, Jorge A. Jiménez-Arango, Andrés F. Zea-Vera, Guillermo González-Manrique, José Vargas, Jorge A. Angarita, Gonzalo Zuñiga, Reydmar Lopez-Gonzalez, Cindy L. Beltran, Karen H. Rizcala, Maria T. Morales, Oscar Pacheco, Martha L. Ospina, Anupama Kumar, David R. Cornblath, Laura S. Muñoz, Lyda Osorio, Paula Barreras, Carlos A. Pardo. Guillain–Barré Syndrome Associated with Zika Virus Infection in Colombia. New England Journal of Medicine, 2016; DOI: 10.1056/NEJMoa1605564

Source: https://www.sciencedaily.com/releases/2016/10/161006092317.htm

Guillain-Barre and CIDP

Guillain-Barré Syndrome | Johns Hopkins Medicine

Guillain-Barre syndrome (GBS) is an acute inflammatory disease of the peripheral nerves. An autoimmune attack on the myelin (insulation around individual nerve fibers, called axons) results in demyelination. Loss of myelin can occur in sensory, motor or autonomic nerves.

Most patients recover spontaneously, but the recovery can be hastened by plasma exchange or intravenous immunoglobulins. In a small number of patients the inflammation in the nerve can be severe enough to cause degeneration of the whole nerve fibers. In those patients, the recovery is often slower and incomplete.

A chronic form of this illness may present with progressive symptoms and result in CIDP (Chronic inflammatory demyelinating polyneuropathy).

Symptoms

GBS patients develop rapidly progressive sensory symptoms such as unusual sensations (paresthesias) and numbness, and motor symptoms such as weakness and cramping in their legs followed by their arms. Patients may also develop weakness of their breathing and difficulty chewing and swallowing.

Difficulty breathing may create a neurological emergency as the patients can develop respiratory arrest. A sizeable number of patients also develop autonomic dysfunction where they experience fluctuations in their blood pressure and cardiac arrhythmias. GBS is one of the true neurological emergencies. Patients need to be monitored closely during the initial acute phase of the illness.

In contrast, CIDP is a slowly progressive illness with diffuse sensory and motor symptoms.

Diagnosis

Diagnosis of GBS and CIDP is history, clinical examination and supporting laboratory investigations. These include electromyography with nerve conduction studies, blood tests and analysis of spinal fluid. In most instances CIDP requires nerve biopsy for histopathological evaluation.

Treatment

GBS patients with respiratory failure require full supportive care in the intensive care unit. Plasma exchange or intravenous immunoglobulins (IVIG) are administered to hasten the recovery from GBS. During the recovery, patients often need aggressive rehabilitation.

CIDP as an autoimmune disease often responds to corticosteroids. However, long-term use of corticosteroids is associated with multiple complications and patients are often switched to “corticosteroid-sparing” agents.

Acute exacerbations of symptoms can sometimes be treated with intravenous immune globulins (IVIG) or plasma exchange. Neuropathic pain due to CIDP can be treated with anti-seizure medications, antidepressants such as, or analgesics including opiate drugs.

In severe painful conditions patients may be referred to the Blaustein Chronic Pain Clinic for a multidisciplinary approach to pain management.

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Johns Hopkins’ Neurosciences Consultation and Infusion Center is open and ready to welcome you at Pavilion II at Green Spring Station in Lutherville, Maryland.

Source: https://www.hopkinsmedicine.org/neurology_neurosurgery/centers_clinics/peripheral_nerve/conditions/guillain_barre_and_cidp.html

NeuroNow – Beating Back Guillain-Barre Syndrome

Guillain-Barré Syndrome | Johns Hopkins Medicine

Date: May 20, 2013

Jeff Dalton, diagnosed with Guillain-Barre syndrome and treated at Johns Hopkins, married his girlfriend, Christina, late last year.

When Jeff Dalton woke up one April morning last year, he immediately knew something was wrong. His legs felt incredibly weak as he swung them bed.

“They felt Jello,” he says. “I’d never experienced anything it.”

The 46-year-old pushed through his workday as a road crew foreman for the Maryland State Highways Administration, even cutting grass on his riding lawn mower when he got home. But the weakness was still there the next morning, and it had taken a turn for the worse. He could barely walk, and his arms and hands felt numb and tingly. 

Worried that he was having a stroke, Dalton headed to a local hospital emergency room with several family members. Tests didn’t turn up an obvious culprit for his problems.

But the doctor he saw did mention the possibility of Guillain-Barre Syndrome (GBS), a condition in which the immune system, for unknown reasons, turns on the insulation that coats nerve fibers.

Because nerves need this insulation to effectively send signals to muscles for movement and from the skin to the brain for sensation, this attack and subsequent destruction can lead to progressive paralysis and loss of feeling. The disease is thankfully rare, affecting only one or two people per 100,000.

The emergency room doctor suggested that Dalton see a neurologist, so he headed home to wait five days until the next open appointment. However, his symptoms quickly grew worse.

Fearing now for his life, Dalton headed to the emergency room at The Johns Hopkins Hospital.

There, doctors led by Department of Neurology Director Justin McArthur confirmed that Dalton indeed had GBS.

“After we admitted him, Jeff went from being weak in the legs to completely paralyzed, losing the ability to speak or swallow within a day,” McArthur says. “To be wide awake and paralyzed is a terrifying experience.”

McArthur and his team soon scheduled Dalton for plasmapheresis, a treatment in which the blood’s plasma is filtered to remove components responsible for triggering the immune response. Dalton received daily treatments over five days.

Initially, the treatments had no effect. When Dalton left Johns Hopkins nearly two weeks after he’d arrived to head to a rehabilitation facility, machines were still breathing for him. One of his eyes drooped completely closed, and the other opened only halfway despite his best efforts.

Dalton was only able to move his feet, and then only barely. With that minimal motion, he was able to communicate with his care providers and family members using a letter board his then-girlfriend had constructed.

With one foot labeled yes and the other no, he painstakingly spelled out words, asking questions, making comments—and eventually proposing to his girlfriend, Christina, who said yes.

Within weeks, Dalton began to make progress. Tracking his care from afar as Dalton proceeded to various rehab and other care facilities, McArthur saw that Dalton began to breathe on his own and become stronger, eventually regaining the ability to take bites from a cheeseburger and take the first steps since he became ill. On December 28, Dalton married Christina.

McArthur, who still sees Dalton every two months, says he expects him to continue to progress, perhaps even coming back fully from this daunting ordeal. “We get used to seeing people respond to antibiotics and other medicines within hours or days,” McArthur says. “Neurological recovery takes a very long time, but this man is determined to recover. His prognosis is quite good.”  

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Source: https://www.hopkinsmedicine.org/news/publications/neuronow/neuronow_summer_2013/beating_back_guillain_barre_syndrome

John Griffin, M.D. (In Memorium)

Guillain-Barré Syndrome | Johns Hopkins Medicine
Back to Leadership

John Griffin, M.D. (In Memorium)

Dr. Griffin was brought up in Nebraska and attended Grinnell College, and Stanford University School of Medicine. He was a medical intern and resident at Stanford, and did his neurology residency at Johns Hopkins, before going to the NIH as a Clinical Associate.

He was on the faculty at Johns Hopkins since 1976, Professor of Neurology and Neuroscience since 1986, and Professor of Pathology since 1999. He was Director of the Department of Neurology and Neurologist-in-Chief at Johns Hopkins from 1999-2006. He was named the Director of the Johns Hopkins Brain Science Institute in 2007. In 2008, Dr.

Griffin was appointed University Distinguished Service Professor in the Department of Neurology, an appointment that has been bestowed on only a select number of faculty. His research career was devoted to the neurobiology and peripheral nerve degeneration and regeneration and to studies of peripheral neuropathies.

Jack’s honors include Jacob Javits Award from the NIH, and multiple teaching awards, including the Professor's Award of the Johns Hopkins University School of Medicine. He gave many named lectures, including the Robert Wartenberg Lecture of the American Academy of Neurology and the Soriano Lecture of the American Neurological Association.

He was a former member of the National Advisory Council to the National Institute of Neurologic Disease and Stroke. He was former Chair of the Burroughs Wellcome Fund Program in Translational Research. He was Past President of the Peripheral Nerve Society, the Society for Experimental Neuropathology, and of the American Neurological Association. Dr.

Griffin was founding Editor-in-Chief of the journal, Nature Clinical Practice Neurology. He was a member of the National Academy of Sciences Institute of Medicine. In 2007, Dr. Griffin was awarded the prestigious Johns Hopkins Heritage Award for his outstanding service to the University.

Dr. Griffin’s career spanned both basic neurologic investigation and translational research. Most recently, the laboratory was focused on three areas: mechanisms of degeneration and of axonal protection in nerve disease, mechanisms underlying painful nerve diseases, and the acquired demyelinating neuropathies. He published over 300 papers in these areas and edited major textbooks on peripheral neuropathies. Dr. Griffin led the initial translational studies of the basis and treatment for Guillain-Barre syndromes. He was an organizer of the North American trial of plasmapheresis for treatment of the Guillain-Barré syndrome, the first demonstration of an effective therapy in this disease. He led a team of investigators from Johns Hopkins, the University of Pennsylvania, Beijing Children's Hospital, and Second Teaching Hospital in Hebei Province, China, in investigating Guillain-Barré syndrome in Northern China. These studies defined an important variant of Guillain-Barré syndrome, Acute Motor Axonal Neuropathy (AMAN). Subsequent studies have identified the role of Campylobacter-jejuni enteritis as an antecedent to the AMAN syndrome, and have dissected the pathology and immunopathology of the disease. It has proved to be a disorder mediated by IgG antibodies against specific nerve gangliosides. The axonal form of GBS is currently one of the best understood examples of “molecular mimicry”, in which the immune response to an infectious organism leads to an immune attack on similar antigens in the nervous system.

In neuropathies, he teamed with Dr. Justin McArthur in the early development of skin biopsies to assess epidermal nerve fibers, showing that these fibers are lost in many painful neuropathies.

He examined the contribution of C-fiber nociceptors to experimental neuropathic pain and the responses of Remak Schwann cells in nerve disease.

Recent studies examined the roles of growth factors in maintenance, degeneration, and regeneration of peripheral nerve fibers.

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Source: https://www.brainscienceinstitute.org/about/leadership/john_griffin

Guillain-Barré Syndrome | Johns Hopkins Medicine

In a collaborative effort with scientists at six Colombian hospitals, Johns Hopkins researchers report what they believe to be the strongest biological evidence to date linking Zika virus infection and Guillain-Barré syndrome.

Epidemiology data have long suggested a close relationship between rising Zika virus infection rates and instances of Guillain-Barré. The new study's results, published online today in The New England Journal of Medicine, support the correlation with immunologic and viral evidence of Zika infection in a substantial number of people with Guillain-Barré, the investigators say.

Guillain-Barré is a very rare but potentially paralyzing disorder of the nervous system that appears days to weeks after infection with viruses or bacteria.

A so-called post-infectious immune condition, it occurs when a person's own immune system attacks the myelin sheaths that protect the body's nerve cells, often resulting in muscle weakness, pain, sensory deficiencies and, in very acute cases, paralysis.

Feature coverage

Guillain-Barré, which affects an estimated one or two 100,000 people after infections, is diagnosed with electrodiagnostic neurological tests that measure the conductive speed and activity of nerve signals. Scientists do not know why it strikes some people and not others.

“At the beginning of the Zika outbreak in South America, my colleagues in Colombia contacted me with concern about the increasing number of patients with neurological complications in their hospitals,” says Carlos A.

Pardo, associate professor of neurology and pathology at Johns Hopkins University's School of Medicine.

Pardo earned his medical degree in Colombia and is an expert in neuroimmune and infectious diseases, including Guillain-Barré.

For the new study, Pardo's team designed strategies with colleagues in Colombia to evaluate patients with suspected neurological problems associated with Zika and provided tools for viral tests of blood, cerebrospinal fluid, and urine samples from 68 people with symptoms of Guillain-Barré. Of the 68 patients initially evaluated in Colombia, virus and immunology studies were conducted using the body fluids from 42. After some evaluation, the researchers found urine to be the most reliable fluid to diagnose Zika infection in patients with Guillain-Barré.

Seventeen patients tested positive for Zika virus in their urine.

Another 18 had no evidence of Zika virus in urine but showed the immunologic footprints of Zika infection through the presence of virus-specific antibodies in their blood or spinal fluid.

Most of the patients were adults—38 were males, and 30 were females of an average of 47 years old. Almost all patients displayed two or more clinical symptoms of Zika infection, which include fever, headache, rash, and conjunctivitis.

The researchers say that almost one-half of the study participants complained of neurologic symptoms within four days of the onset of Zika symptoms—an unusually fast response, they say, compared to that of people who develop Guillain-Barré symptoms after other viral infections, such as influenza and herpesviruses.

Tests also revealed that most of the 46 patients whose Guillain-Barré was confirmed by electrodiagnostic neurological tests had the acute inflammatory demyelinating polyneuropathy variant of the disorder. This type of Guillain-Barré attacks the myelin, a protective group of cells that insulates the surface of the nerve fibers, the plastic coating on a copper wire.

Pardo says the study is believed to be the largest of its kind to document the role of Zika infection in increased rates of Guillain-Barré so far. He cautions that although the study demonstrates a biological and viral association between Zika infection and Guillain-Barré, it does not reveal the biological mechanisms through which Zika might initiate an immune attack on the nerves.

The research team, he says, continues to collect clinical data and samples from the Colombian hospitals' patients, but the work is constrained by the limited availability of resources, which is further strained by the severe and ongoing Zika outbreak in South America.

Posted in Health

global health, epidemiology, neurology, zika virus

Source: https://hub.jhu.edu/2016/10/05/zika-virus-guillain-barre-syndrome-biological-link/

Guillain–Barré Syndrome Associated with Zika Virus Infection in Colombia | NEJM

Guillain-Barré Syndrome | Johns Hopkins Medicine

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Guillain-Barré Syndrome

Guillain-Barré Syndrome | Johns Hopkins Medicine

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Guillain-Barré syndrome (GBS) is also called acute inflammatory demyelinating polyradiculoneuropathy (AIDP).

It is a neurological disorder in which the body's immune system attacks the peripheral nervous system, the part of the nervous system outside the brain and spinal cord. The onset of GBS can be quite sudden and unexpected and requires immediate hospitalization.

It can develop over a few days, or it may take up to several weeks with the greatest weakness occurring within the first couple of weeks after symptoms appear.

GBS is rare, affecting about 3,000 people in the U.S. It can affect people at any age and both men and women equally. GBS often develops after a respiratory or gastrointestinal viral infection.

What causes Guillain-Barré syndrome?

It’s not clear why some people get GBS. What is known is that the body's immune system begins to attack the body itself.

Normally, the cells of the immune system attack only foreign material and invading organisms, but in GBS, the immune system starts to destroy the myelin sheath that surrounds the axons of many nerve cells, and, sometimes, the axons themselves.

When this occurs, the nerves can’t send signals efficiently, the muscles lose their ability to respond to the commands of the brain, and the brain receives fewer sensory signals from the rest of the body. The result is an inability to feel heat, pain, and other sensations.

GBS can occur after a viral infection, surgery, injury, or a reaction to an immunization.

What are the symptoms of Guillain-Barré syndrome?

These are the most common symptoms of GBS. But each person may have slightly different symptoms.

The first symptom includes weakness or tingling sensations in the legs. This sometimes spreads to the arms and upper body. A neurological exam usually reveals a loss of all deep tendon reflexes. The symptoms may get worse.

In some cases, you may not be able to use your muscles at all. You become paralyzed, and breathing is hard. Your blood pressure and heart function are affected. GBS is a medical emergency and needs to be treated promptly.

Although symptoms can become life-threatening, partial recovery is possible from even the most severe cases of GBS. But you may always have some degree of weakness.

The symptoms of GBS may look other health conditions. Always talk with your healthcare provider for a diagnosis.

How is Guillain-Barré syndrome diagnosed?

The signs and symptoms of GBS vary. It can be difficult to diagnose in its earliest stages.

These signs and symptoms are unique to GBS:

  • Symptoms on both sides of the body
  • Symptoms appear quickly–days or weeks instead of months
  • Loss of reflexes
  • High protein level in cerebral spinal fluid. This is the fluid that surrounds the spinal cord and brain.

To diagnose GBS, you may have the following tests:

  • Spinal tap (lumbar puncture). A special needle is placed into the lower back, into the spinal canal. This is the area around the spinal cord. The pressure in the spinal canal and brain can then be measured. A small amount of cerebral spinal fluid (CSF) can be removed and sent for testing to find out if there is an infection or other problems.
  • Electrodiagnostic tests, such as electromyography (EMG) and nerve conduction velocity (NCV). These studies are done to evaluate and diagnose disorders of the muscles and motor neurons. Electrodes are inserted into the muscle, or placed on the skin overlying a muscle or muscle group, and electrical activity and muscle response are recorded.

How is Guillain-Barré syndrome treated?

There is no known cure for GBS. The goal of treatment is to prevent breathing problems and relieve symptoms. You will need to stay in the hospital for treatment. Medicines are used to control pain and other conditions that may be present.

In addition, you may get treatments, such as plasmapheresis or immunoglobulin, to suppress the immune system and reduce inflammation caused by the immune system’s response to the disease.

  • Plasmapheresis is a procedure that removes the plasma (liquid part of the blood) and replaces it with other fluids. Antibodies are also removed with the plasma, which is thought to help reduce the symptoms of the disease.
  • Immunoglobulin is a blood product that helps to decrease the immune system’s attack on the nervous system.

Other therapies include hormonal therapy and physical therapy (to increase muscle flexibility and strength).

Through research, new treatments for GBS are continually being identified.

Key points about Guillain-Barré syndrome

  • Guillain-Barré syndrome (GBS) is a neurological disorder in which the body's immune system attacks part of the peripheral nervous system.
  • The onset can be quite sudden and unexpected and requires immediate hospitalization.
  • The first symptoms include varying degrees of weakness or tingling sensations in the legs, which, sometimes, spreads to the arms and upper body.
  • The goal of treatment is to prevent breathing problems and relieve symptoms.
  • Recovery can be lengthy and residual muscle weakness or paralysis can occur.

Next steps

Tips to help you get the most from a visit to your healthcare provider:

  • Know the reason for your visit and what you want to happen.
  • Before your visit, write down questions you want answered.
  • Bring someone with you to help you ask questions and remember what your provider tells you.
  • At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also write down any new instructions your provider gives you.
  • Know why a new medicine or treatment is prescribed, and how it will help you. Also know what the side effects are.
  • Ask if your condition can be treated in other ways.
  • Know why a test or procedure is recommended and what the results could mean.
  • Know what to expect if you do not take the medicine or have the test or procedure.
  • If you have a follow-up appointment, write down the date, time, and purpose for that visit.
  • Know how you can contact your provider if you have questions.

Source: https://www.hopkinsmedicine.org/health/conditions-and-diseases/guillainbarr-syndrome