Guillain-Barre Syndrome (GBS) (Described Concisely)

our topic today is guillain-barre syndrome or TBS guillain-barre is classified as an acute polyneuropathy which describes that it comes out of roughly and progresses quickly to damage peripheral nerves the disease may hinder movement sensation or organ function depending on which nerves are involved GBS is a rare condition with an incidence of only 1 to 2 cases per 100,000 people worldwide each year but it is the most common cause of sudden onset flaccid paralysis in developed countries it affects both genders equally GBS was named after French neurologist georgeous Guillen in John Alexander Bray who first observed the syndrome in a patient in 1916 damage to myelin and peripheral axons in GBS is usually first manifested in the hands or feet with symptoms such as paresthesias which include tingling and numbness as the syndrome progresses the dominant features become muscle weakness that progressively worsens to flaccid paralysis as well as absent deep tendon reflexes since electrical signals must travel the farthest to reach the arms and legs symptoms of paresthesias and muscle weakness appear first in the hands and feet and then ascend upwards hence the descriptive term toes to nose is used the symptoms are also experienced symmetrically which means on both sides of the body the patient may or may not experience pain if they do it is most often located in the back shoulders and thighs and may even become quite severe with just slight movements as mentioned the symptoms of muscle weakness can progress until the patient experiences a flaccid paralysis in 25% of patients this weakness affects respiratory muscles and causes respiratory inadequacy a lower percentage experienced respiratory failure in death also nerves of the autonomic nervous system or ans may be affected leading to urinary retention flushing of the face cardiac arrhythmias and orthostatic hypotension the rate that GBS progresses and becomes more severe varies among individuals some progress rapidly over hours while others progress over days or weeks in most patients maximum muscle weakness occurs at two to three weeks after onset of first symptoms lots of times it isn't known what causes GBS but it often follows a gastrointestinal infection with diarrhea or a respiratory tract infection such as a sore throat in the three to six weeks prior to the commencement of symptoms like tingling or weakness the gastrointestinal infections that precede GBS are most often Campylobacter jejuni infections Campylobacter jejuni is one of the most common causes of gastroenteritis resulting from food poisoning and is transmitted by ingesting poorly cooked meat or poultry unpasteurized milk and contaminated drinking water less commonly respiratory tract infections caused by cytomegalovirus epstein-barr virus and mycoplasma pneumoniae precede the onset of guillain-barre a occasionally surgery will precede the syndrome and is less common there are a significant number of cases where patients have reported receiving a flu vaccination prior to development of the syndrome despite this the benefits for receiving the flu vaccine away the small risk for developing GBS after receiving the vaccination there are two main subtypes of GBS the de myelinating form is known as a IDP or acute inflammatory demyelinating polyneuropathy with a IDP the complement system is activated as well as t-cells which activate macrophages that in turn damage the myelin the other main form is the axonal type known as a ma n or acute motor axonal neuropathy with a ma and the damage is mediated mainly by IgG antibodies and complement against the axial lemma both forms result in injury to peripheral neurons the pathophysiology of the axonal form of GPS or AMA n is possible because the capsule of Campylobacter jejuni and certain viruses like CMV and EBV contain antigens that are similar in structure to the portions of the axial lemma of neurons these portions of axial Emin are called gangliosides such as GM 1 and GD 1 the mounted immune response against Campylobacter jejuni or the formation viruses produces antibodies the cross-react with a structurally similar gangliosides in the axons of neurons themselves this cross reactivity is termed molecular mimicry with the AI DP subtype it is mainly the activated T helper cells then activate macrophages that do much of the damage to neurons myelin and schwann cells GBS can be difficult to diagnose but the physician will note the symptoms appear on both sides of the body and that reflexes like the knee-jerk reflex are absent also CSF from a spinal tap will reveal higher than normal levels of protein often greater than 0.5 5 grams per liter due to all the inflammation and white blood cells will be less than 10 per cubic millimeter of CSF these two CSF findings are important to distinguish GBS from lymphoma and polio myelitis which both reveal elevated protein and elevated white blood cells in the CSF neural physiology studies such as nerve conduction studies or NCS and electromyography or EMG are not required for diagnosis but help distinguish from other causes of acute muscle weakness nerve conduction velocity can be measured by placing electrodes on the skin at different locations the electrode stimulates the nerve and the other electrode picks up the electrical activity in the nerve the distance between the electrodes and the time to transmit the impulse between the electrodes can be measured with GPS conduction times are usually slower electromyography test the responsible muscle in response to a nerve stimulation of that muscle in the acute phase of GBS EMG studies often show decreased recruitment of muscles with even rapidly firing motor units in addition to the subtypes a IDP and a ma n other variants of GBS include a msan EMFs and the fringe of cervical brachial variant the table shows manifestations demographics and the antibodies associated with each subtype treatment of GBS includes plasmapheresis also called plasma exchange this process removes antibodies and other immune mediators from the blood that contribute to the destruction of neurons immunoglobulins obtained from a collection of large number of donors may be given IV these immunoglobulins will act to clear damaging immune substances from circulation corticosteroids are not given because they may actually make symptoms worse patients with inadequate ventilation are placed on Meccano ventilation for this reason GBS patients are often treated in the ICU the risk for pneumonia and other infections is greater in patients that are paralyzed so appropriate IV antibiotic therapy may be given caregivers also may manually move the patient's limbs to keep blood flowing and reduce the risk of blood clot formation these patients are immobile which increases the risk for developing the clots some patients may even require anticoagulant therapy to prevent deep vein thrombosis abbreviated DVT when the paralysis improves physical and occupational therapy begins many patients may also need psychological counseling and it is difficult to adjust to the sudden paralysis roughly 2 to 5% of GBS patients die from respiratory paralysis cardiac arrest or related problems but gratefully most patients can expect to have a full recovery this happens as the nerves remyelination and may take up to between 6 and 12 months however up to 30% of GBS patients still have residual weakness after 3 years and about 3% have weakness and tingling many years later in summary please remember that the peripheral neuropathy associated with GBS comes on with a sudden onset this syndrome is autoimmune demyelinating and descending meaning it starts in the hands and feet and moves upward it is also a symmetrical condition meaning that symptoms occur on both sides of the body or both left and right limbs at the same time it affects both sensory and motor neurons and symptoms include paresthesias absent reflexes pain and muscle weakness that may progress to affect respiratory muscles ans features include cardiac arrhythmias and orthostatic hypotension due to these features GBS is considered a medical emergency findings that support a positive diagnosis for GBS include the aforementioned symptoms high levels of protein and low levels of leukocytes in the CSF and positive results on neural physiology studies like nerve conduction studies and electromyography the main treatments for GBS include plasmapheresis immunoglobulin antibiotics and anticoagulant therapies as well as supportive measures since the syndrome may be life-threatening after the acute phase physical occupational and psychological therapies are necessary in conclusion please answer the following question you may pause the video to think of your answer if you answer J than you are correct for selection one to be true it would need to say peripheral nerves instead of CNS tracks for selection - it should say flaccid paralysis not paralysis for selection three to be true it should say most patients have a full recovery for selection for GBS has been linked to several pathogens but not Clostridium Campylobacter jejuni is the main pathogen thanks for watching

Channel: PhysioPathoPharmaco

Views: 457,507

Keywords: Guillaine-Barre, video, animation, cartoon, GBS, pathophysiology, pathogenesis, symptoms, diagnosis, treatment, paralysis, respiratory failure

Id: 7vmZVNmAYf4

Length: 12min 29sec (749 seconds)

Published: Tue Nov 28 2017