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Gullian Barre Syndrome.pptx
- 1. GUILLAIN BARRE SYNDROME AASHISH GHOSHRESTHA MPT NEURO
- 2. CONTENTS • Introduction • Incidence •Etiology • Clinical Manifestation • Classification • Diagnosis • Management
- 3. INTRODUCTION • Acute inflammatory,demyelinating immune - mediated polyneuropathy(AIDP) • Landry’s Palsy • It affects the nerve roots and peripheral nerves, leading to the motor neuropathy and flaccid paralysis with possible sensory and ANS effect. • Approximately 27% of the patient with GBS have no identified preceding illness, however, more than two thirds had symptoms of an infectious disease 1 to 3 weeks before the onset of the GBS syndromes. • GBS usually has a good prognosis • Named after the French Neurologist Georges Guillain and Jean Alexandre Barre in 1916.
- 4. INCIDENCE • The incidenceof GBS is1-3 cases per 100,000 person world wide • Male:female::2:1 • In developed countries, it is the most common cause of the sudden onset flaccid paralysis.
- 5. ETIOLOGY • The exactreason of the GBS is not known. • One of the causes is GI infection with diarrhea. • GI tract infection is caused due to Campylobacter jejuni (i.e gastroenteritis), resulting for the food poisoning and transmitted by ingesting poorly cooked meat, unpasteurized milk or contaminated drinking water. • Another is related to the respiratory tract infection caused by Mycoplasma pneumoniae, Epstein Barr Virus or Cytomegalovirus. • Occasionally it can be following surgeries • Or it can be following after receiving vaccination(chance is very low)
- 6. PATHOPHYSIOLOGY • In GBS/AIDP, the spinal roots and peripheral nerve are infiltrated with macrophages and T-helper lymphocytes. • Macrophages then attack the strip of the myelin sheaths. • In milder cases of the GBS the axon are left intact and the nerve are reinnervated, typically in a matter of weeks. • Similarly in the acute motor axonal neuropathy(AMAN), macrophages invade the axon directly, leaving the myelin sheath intact by the process called “molecular mimicry.” It is related to long lasting or permanent muscular weakness.
- 8. CLINICAL MANIFESTATION • Itis characterized by the rapidly evolving, relatively symmetrical ascending weakness or flaccid paralysis. • Motor impairment may vary from mild weakness of the distal lower extremity musculatures to the complete paralysis of the peripheral, axial, facial and extraocular musculature • There is areflexia or absence of the deep tendon reflex. • 38% to 86% of patient with GBS are present with severe fatigue depending upon the cutoff point used to define severity and the age of the sample. • 20% to 38% of patient may end up with the respiratory muscle weakness or respiratory inadequacy and very low percentage in that die of respiratory failure and even death.
- 9. • Sensory symptoms:distal hyperesthesia, paraesthesias, numbness, and decreased vibratory or proprioception • ANS symptoms: urinary retention, flushing of face, arrhythmia, and orthostatic hypotension • Some experience pain mainly at the back, shoulder, thighs and may even increase by the slight movements. • Some patient develop cranial nerve involvement, primarily facial muscle weakness, also may develop oropharyngeal and oculomotor involvement
- 10. DIAGNOSTIC CRITERIA OFGBS • Motor weakness are progressive, symmetrical and usually progression is distal to proximal which is either self limiting or may extend to the quadriplegia with respiratory and cranial nerve involvement and presence of the areflexia • Mild sensory symptoms or signs, particularly paresthesia and hyperesthesia • Autonomic disfunction such as tachycardia and arrhythmias, vascular symptoms • Absence of fever on the onset of symptoms, history of flulike illness common • Laboratory result showing rise in the protein level and reduction of the mononuclear leukocytes • Electrodiagnostic testing, NCV is usually abnormal. • Recovery usually begins 2-4 weeks after the plateau of disease process
- 11. CLASSIFICATION OF GBS •Acute Inflammatory Demyelinating Polyneuropathy • Acute Motor Axonal Neuropathy • Acute Motor Sensory Axonal Neuropathy • Miller Fisher Syndrome • Acute Autonomic Neuropathy • Chronic Inflammatory demyelinating Polyradiculoneuropathy
- 13. DIAGNOSIS • Can bedifficult • CSF from the spinal tap shows higher protein level usually greater than 0.55gm/ liters(0.15-0.6gm/lt) and WBC less than 10/ cubic meter(200-400/ cubic meter) of CSF • Increased WBC means chances of lymphoma or poliomyelitis • Electrodiagnostic testing like NCV and EMG to rule out other acute muscular weakness. • Slow conduction in NCV • Decreased recruitment of muscle with even rapidly firing motor units
- 14. MANAGEMENT • Medical management: •Plasmapheresis • Immunoglobulins • Mechanical ventilation for respiratory muscle weakness • IV antibiotic therapy • Anticoagulants to prevent blood clotting and DVT
- 15. THERAPEUTIC MANAGEMENT • Providingmoral support at the acute phase • Prevention of long term medical comorbidities during acute through the early recovery • Rehabilitation throughout recovery phase
- 16. EXAMINATION • HISTORY: • Patternand sequence of symptom onset • Presence of illness or injury or prior episodes of sensorimotor problems. • MOTOR FUNCTION: • Observe muscle bulk and function • DTR to rule out the reflexes • MMT identifying the pattern of weakness(serial recording of the specific muscle) • Cranial nerve examination • ROM examination • Equilibrium examination in standing if possible • Current functional status(ADL, B n B)
- 17. • SENSORY SYSTEM •To identify the pattern of sensory loss or changes • To identify the specific type of sensory changes • Identification of pain type and location • Identification of pressure point to prevent from pressure point • AUTONOMIC SYSTEM • BP at rest and after exercise(orthostatic hypotension) • HR at rest and after exercise(arrhythmias) • Body temperature • Bowel and Bladder control
- 18. • PSYCHOSOCIAL SYSTEMS: •Identify the family members and make them aware about the long term issues • ELECTRODIAGNOSTIC TESTING: • NCV • EMG • RESPIRATORY AND DYSPHAGIA EXAMINATIONS • Maintain FVC and Oxygen Saturation
- 19. • Therapeutic InterventionGoals: • Facilitate resolution of respiratory problems and dysphagia • Minimize pain • Prevent contractures, decubitus ulcers, and injury to weakened or denervated nerve • Introducing graduated program of active exercise while monitoring overuse and fatigue • Resume psychological roles and improve quality of life
- 20. • FACILITATE RESOLUTIONOF RESPIRATORY PROBLEMS AND DYSPHAGIA • Focus mainly on the increase ventilation, reduce oxygen consumption, control secretions and improve exercise tolerance. • Chest percussions • Breathing exercises • Spirometry • Strick protocol to prevent overfatigue while weaning from mechanical ventilation • In severe cases, speech therapist for dysphagia
- 21. • MINIMIZE PAIN •TENS to desensitization whose pain is not reduced by passive movements or pain medications • PREVENT CONTRACTURES, DECUBITUS ULCERS, AND INJURY TO WEAKENED OR DENERVATED NERVE • Positioning and Passive range of motion in acute stage. Proper maintenance of the physiological position of hands and feet. • Continuous stretch maintained for 20 minutes • Use of splints for prolonged positioning • ROM exercises to increase circulation, provide lubrication of the joints and maintain the extensibility of the capsule, muscles and tendon tissues • Continuous passive movements can be beneficial for maintaining the joint range • Massage to maintain muscle tissue mobility and tissue nutrition.
- 22. • INTRODUCING GRADUATEDPROGRAM OF ACTIVE EXERCISE WHILE MONITORING OVERUSE AND FATIGUE • In acute stage active exercise is limited to the pain free range or absence of fatigue • After the strength is improved low resistance activities until MMT is 3/5 with frequent rest and avoiding fatigue • In case of soreness or weakness additional activities should not be initiated