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1、Guillain Barr Syndrome and the influenza vaccineTed M. Burns, MD Associate Professor, Neurology University of VirginiaOrly Avitzur, MD Associate Professor, Neurology New York Medical CollegeLearning ObjectivesUpon completion of participation, participants will be able to: Discuss the clinical featur
2、es of GBS, its pathogenesis and treatment options Be aware of prior associations between GBS and influenza vaccines Know when and how to report to VAERS Understand the risks of underreportingDisclosures Dr. Avitzur and Dr. Burns have nothing to disclose. Accreditation Statement The AAN is accredited
3、 by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.AMA PRA Category 1 Credit The AAN designates this educational activity for a maximum of 1 (one) AMA PRA Category 1 Credit. Physicians should only claim credit commensurate with the e
4、xtent of their participation in the activity.Outline1. Overview of Guillain-Barre Syndrome (GBS) 2. Influenza vaccine and GBS 3. VAERS Outline1. Overview of Guillain-Barre Syndrome (GBS) 2. Influenza vaccine and GBS 3. VAERS Clinical features classic GBSMotor sensory polyradiculoneuropathy1.Weakness
5、 2.Positive neuropathic sensory symptoms tingling, pain3.Areflexia (or hyporeflexia)4.Diaphragmatic and cranial nerve weakness 50%5.Autonomic involvement 50% Acute-to-subacute onsetNadir within 4 weeksMonophasic illnessSeminars Neurol 2008;28:152-167Clinical features classic GBSMotor sensory polyrad
6、iculoneuropathy1.Weakness 2.Positive neuropathic sensory symptoms tingling, pain3.Areflexia (or hyporeflexia)4.Diaphragmatic and cranial nerve weakness 50%5.Autonomic involvement 50% Acute-to-subacute onsetNadir within 4 weeksMonophasic illnessSeminars Neurol 2008;28:152-167Classic GBS: clinical fea
7、turesInitial presentation (%)Nadir (%)Paresthesias7085Weak UE20 90Weak LE6095Weak face3560Weak swallow2550Sphincter155Ataxia1015Areflexia7590Sensory loss4075Ventilator1030CSF Pro 555090Ropper AH, The Guillain-Barre syndrome, NEJM 1992;326:1130-1135Classic GBS: clinical featuresInitial presentation (
8、%)Nadir (%)Paresthesias7085Weak UE20 90Weak LE6095Weak face3560Weak swallow2550Sphincter155Ataxia1015Areflexia7590Sensory loss4075Ventilator1030CSF Pro 555090Ropper AH, The Guillain-Barre syndrome, NEJM 1992;326:1130-1135Classic GBS: clinical featuresInitial presentation (%)Nadir (%)Paresthesias7085
9、Weak UE20 90Weak LE6095Weak face3560Weak swallow2550Sphincter155Ataxia1015Areflexia7590Sensory loss4075Ventilator1030CSF Pro 555090Ropper AH, The Guillain-Barre syndrome, NEJM 1992;326:1130-1135AMANVariantsAMSANMFSSeminars Neurol 2008;28:152-167Antecedent infection in two-thirds Respiratory infectio
10、n diarrheaJacobs BC, Rothbarth PH, van der Meche FG, et al. Neurology 1998;51:1110-1115. Infectious agent: C. jejuni CMV, EBVJacobs BC, Rothbarth PH, van der Meche FG, et al. Neurology 1998;51:1110-1115. Diagnosis: consider mimics of GBS Acute myelopathy: corticospinal tract findings, back pain Vasc
11、ulitic neuropathy: Systemic symptoms, pain, asymmetry Thiamine deficiency: Alcohol abuse, s/p bariatric surgery West Nile poliomyelitis: lower motor neuron, fever, meningitis, pleocytosis Lyme neuroborreliosis: polyradiculitis, rash, systemic symptoms Tick paralysis: children, pure motor (low CMAPs)
12、 Botulism: oculobulbar, motor, nausea/vomiting/constipation Acute intermittent porphyria: GI symptoms, autonomic crisis Heavy metals, acute: systemic, GI symptoms, skin Organophosphates: insecticide exposure, cramps, axonopathy n-Hexane: glue- and gasoline-sniffers Poliomyelitis: lower motor neuron,
13、 fever, meningitis, pleocytosis Buckthorn toxin: berries of buckthorn shrub, 1-3 weeks later; SW US CMV polyradiculopathy: advanced AIDS, pleocytosis Diphtheria: 2-3 months after pharyngitis Marine toxins: pufferfish, shellfishSeminars Neurol 2008;28:152-167Diagnosis: CSF in GBSCSF protein abnormal
14、initially in 60%Dont let normal CSF during first week dissuade you from treating early After first week, protein is almost always elevated 90% “in fully developed illness” Few WBCs (10)Ropper AH, NEJM 1992;326:1130- 1136; Al-Shekhlee et al, Muscle Nerve 2005;32:66-72.Diagnosis: EDX in early GBS 1. F
15、requently abnormal: H reflex, F waves, low distal CMAP amplitude, dispersion of CMAP, prolonged distal latencies “Sural sparing” pattern on sensory NCS 2. Often normal in early GBS: Conduction block and temporal dispersion on motor NCS Non-uniform slowing on motor NCSGordon PH, Wilbourn AJ. Arch Neu
16、rol 2001;58:913-917; Albers et al, Muscle Nerve 1985;8:528-539; Al-Shekhlee et al. Muscle Nerve 2005;32:66-72Pathogenic events of early GBS1. Otherwise trivial infection1. Otherwise trivial infectionJacobs BC, Rothbarth PH, van der Meche FG, et al. Neurology 1998;51:1110-1115. Pathogenic events of early GBS1. Otherwise trivial infection 2. Molecular mim
