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Guillain barré syndrome
- 1. Guillain-Barré syndrome Dr. AngeloSmith M.D WHPL
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- 3. It has anannual incidence of 0.6 to 2.4 cases per 100,000 population and occurs at all ages and in both sexes With the marked decline in the incidence of polio, Guillain-Barré syndrome is now the most common cause of acute flaccid paralysis in healthy people is an acute inflammatory demyelinating polyneuropathy characterized by progressive muscle weakness and areflexia
- 4. Guillain-Barre’ Syndrome Post-infectiouspolyneuropathy; ascending polyneuropathic paralysis An acute, rapidly progressing and potentially fatal form of polyneuritis
- 5. Guillain-Barre’ Syndrome Affectsthe peripheral nervous system
- 7. PATHOGENESIS Peripheral nerve demyelinationin Guillain-Barré syndrome is believed to be immunologically mediated Humoral factors and cell-mediated immune phenomena have been implicated in the damage of myelin and/or the myelin-producing Schwann cells
- 9. Guillain-Barre’ T-cell sensitization occurswhich causes loss of myelin which disrupts nerve impulses Loss of myelin, edema and inflammation of the affected nerves, causes a loss of neurotransmission to the periphery. 85% of patients recover with supportive care.
- 11. Guillain-Barré syndrome hasbeen reported to follow vaccinations epidural anesthesia thrombolytic agents It has been associated with some systemic processes, such as Hodgkin's disease SLE Sarcoidosis, and infection with Campylobacter, Lyme disease, EBV, CMV, HSV, mycoplasma, and recently acquired HIV infection
- 12. Campylobacter infection is themost commonly identified precipitant of Guillain-Barré syndrome A case-control study involving 103 patients with the disease found that 26% of affected individuals had evidence of recent C. jejuni infection compared with 2% of household and 1% of age-matched controls Seventy percent of those infected with C. jejuni reported a diarrheal illness within 12 weeks before the onset of the neurologic illness
- 15. Clinical Manifestations Usuallydevelop 1 to 3 weeks after URI or GI infection Weakness of lower extremities (symmetrically) Parathesia (numbness and tingling), followed by paralysis Hypotonia and areflexia (absence of reflexes) Pain in the form of muscles cramps or hyperesthesias (worse at night).
- 16. Early in thecourse, patients frequently complain of aching or sciatica-like lower back or leg pain At some point during their illness, up to 25 percent of patients require mechanical ventilation More than 90% of patients reach the nadir of their function within two to four weeks, with return of function occurring slowly over weeks to months
- 17. Two-thirds of patientsdevelop the neurologic symptoms 2-4 weeks after what appears to be a benign respiratory or gastrointestinal infection The initial symptoms are fine paresthesias in the toes and fingertips, followed by lower extremity weakness that may ascend over hours to days to involve the arms, cranial nerves, and in severe cases the muscles of respiration
- 18. Clinical manifestations Autonomic nervoussystem dysfunction results from alterations in sympathetic and parasympathetic nervous systems. Results in respiratory muscle paralysis, hypotension, hypertension, bradycardia, heart block, asystole. Involvement of lower brainstem leads to facial and eye weakness
- 20. Physical Examination Symmetriclimb weakness with diminished or absent reflexes Minimal loss of sensation despite paresthesias Signs of autonomic dysfunction are present in 50 percent of patients, including Cardiac dysrhythmias (asystole, bradycardia, sinus tachycardia, and atrial/ventricular tachyarrhythmias) Orthostatic hypotension Transient or persistent hypertension Paralytic ileus Bladder dysfunction Abnormal sweating
- 21. DIAGNOSTIC STUDIES Electrophysiologic studiesare the most specific and sensitive tests for diagnosis of the disease They demonstrate a variety of abnormalities indicating evolving multifocal demyelination Slowed nerve conduction velocities Partial motor conduction block Abnormal temporal dispersion Prolonged distal latencies A normal study after several days of symptoms, makes the diagnosis of Guillain-Barré syndrome unlikely
- 22. DIAGNOSTIC STUDIES After thefirst week of symptoms, analysis of the cerebrospinal fluid (CSF) typically reveals normal pressures few cells (typically mononuclear) an elevated protein conc. (greater than 50 mg/dL) Early in the course (less than one week), protein levels may not yet be elevated, but only rarely do they remain persistently normal If CSF pleocytosis is noted, other diseases associated with Guillain-Barré syndrome eg, HIV infection, Lyme disease, malignancy, and sarcoidosis should be considered
- 23. Therapeutic management Ventilatorsupport! Plasmapheresis used within the first 2 weeks of onset. If treated within the first 2 weeks, LOS of morbidity is reduced. After three weeks, plasmapharesis no benefit. IV immunoglobin Nutritional support (TF, TPN, Diet)
- 26. Variants Acute inflammatory demyelinating polyneuropathy(AID P) is the most common form of GBS, and the term is often used synonymously with GBS. It is caused by an autoimmune response directed against Schwann cell membranes.
- 27. Miller Fisher syndrome(MFS) is a rare variant of GBS. Accounting for about 5% of GBS cases, it manifests as a descending paralysis, proceeding in the reverse order of the more common form of GBS.
- 28. Acute motoraxonal neuropathy (AMAN), also known as Chinese paralytic syndrome, attacks motor nodes of Ranvier and is prevalent in China and Mexico. It is probably due to an auto-immune response directed against the axoplasm of peripheral nerves.
- 29. Acute motor sensoryaxonal neuropathy (AMSAN) is similar to AMAN, but also affects sensory nerves with severe axonal damage. Acute panautonomic neuropathy is the rarest variant of GBS, sometimes accompanied by encephalopathy.
- 30. Bickerstaff's brainstem encephalitis (BBE),a further variant of Guillain–Barré syndrome, is characterized by acute onset of ophthalmoplegia, ataxia, disturbance of consciousness, hyperreflexia or Babinski's sign.