POSTINFECTIOUS NEUROPATHIES

POLIOVIRUSES Member of enteroviruses  Picornoviridae family. There are 3 antigenically distinct serotypes of poliovirus (1,2,3) The neuropathy of poliomyelitis and other paralytic disease caused by nonpolio enteroviruses (coxsackie, echoviruses) is due to direct cellular destruction

POLIOVIRUSES Secondary damage may be due to immunologic mechanism. In poliomyelitis (PM) neuronal lesions occur : Spinal cord (chiefly in the anterior horn cell) Medulla Cerebellum Midbrain Thalamus and hypothalamus Pallidum Cerebral cortex

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POLIOVIRUSES Clinical manifestations 1) Inapparent infection: Causes no disease, no sequela 2) Abortive PM: Brief febrile illness. Malaise, anorexia, nausea, vomiting, sore throat constipation, diffuse abdominal pain. 3) Nonparalytic PM: headache, nausea, vomiting, are more intense. Stiffness of the post. muscles of the neck, trunk and limbs. Nuchal rigidity. Head drop. Weakness  changes in reflexes

POLIOVIRUSES Superficial reflexes  are usually the first to be diminished. (cremasteric and abdominal) Changes in deep tendon reflexes occur 8-24 hr after the superficial reflexes are depressed. SENSORY DEFECTS DO NOT OCCUR!

POLIOVIRUSES 4) Paralytic PM: Nonparalytic PM + waekness of one / more muscle group These symptoms may be followed by a symptom free interval of several days and the recurrence of disease Bladder paralysis lasting 1-3 days occurs approximately 20 % of patients.

POLIOVIRUSES Flaccid paralysis: most obvious clinical expression. Muscular atrophy  denervation + atrophy of muscle Respiratory and cardiac arythmias, blood pressure and vasomotor changes Spinal form: weakness of some of the muscles of neck, abdomen, trunk, diaphragm, thorax, extremities. Bulbar form: weakness in the motor distrubition of one / more cranial nerves Bulbospinal form: combined form Encephalitic form: irritability, disorientation, drowsiness

POLIOVIRUSES A number of components acting together. İnsufficiency of ventilation : hypoxia, hypercapnia Diagnosis: combination of fever + headache + neck and back pain + asymetric flaccid paralysis + pleocytosis 200-300 cells/mm³ : PNL (early)  mononuclear. CSF protein is normal or slightly elevated at the onset rises between 500-1000 mg/dl by the second week.

POLIOVIRUSES Serologic testing. Poliovirus is cultured from the stool, naso-pharynx, CSF. Treatment Abortive: supportive, analgesic, sedatives, bedrest. Nonparalytic : relief for discomfort of muscle tightness and spasm of neck, trunk and extremities. Analgesics + hot packs. Footboard. Gentle physical therapy.

POLIOVIRUSES Paralitic: require hospitalization. Calm atmosphere. Active / passive motions. Opiates and sedatives. Pure bulbar: tracheostomy. Mechanical ventilation. Complications: melena, acute gastric dilatation, mild hypertension, cardiac irregularities, acute pulmonary edema, skeletal decalcification  hypercalciuria.

POLIOVIRUSES Prevention vaccination IPV. OPV – vaccine of choice in countries where polio is endemic. Paralysis on the basis of anterior horn cell disease occasionaly results from infection with nonpolioviruses many coxackieviruses and echoviruses have been associated with the GUILLAIN BARRE SYNDROME

GUILLAIN-BARRE SYNDROME Postinfectious polyneuropathy causes demyelination in mainly motor but sometimes also sensory nerves. Affects people of all ages and not hereditary.Paralysis usually follows a nonspesific viral infection by abaut 10 days (camphylobacter jejuni, mycoplasma pneumoniae) Weakness begins usually in the lower extremities and progressively involves the trunk, the upper limbs and finally bulbar muscles.

GUILLAIN-BARRE SYNDROME Proximal and distal muscles are involved symmetrically Onset is gradual and progresses over days and week. Weakness  inability to walk  flaccid tetraplegia Paresthesias Bulbar involvoment  ½ of cases. Respiratory insufficiency may result.

GUILLAIN-BARRE SYNDROME Dysphagia and facial weakness are often impending signs of respiratory failure Urinary incontinance or retention of urine is transient. Tendon reflexes are lost usually early in the course but are sometimes preserved until later.Clinical course is usually benign and spontaneous recovery begins within 2-3 wks. Lability of blood pressure and cardiac rate, postural hypotension ,bradycardia.

GUILLAIN-BARRE SYNDROME Congenital GB syndrome : Rare Generalized hypotonia Weakness Areflexia No evidence of residual disease by a year of age.

GUILLAIN-BARRE SYNDROME Diagnosis: CSF: protein is elevated to more than twice the upper limit of normal. Glucose  Normal No pleocytosis The dissociation between high CSF protein and a lack of cellular response in a patient with an acute or subacute polyneuropathy is diagnostic of GBS

GUILLAIN-BARRE SYNDROME EMG: Evidence of acute denervation of muscle. Serum CK: mildly elevated/N Treatment: rapidly progressive ascending paralysis is treated with IVIG adm 2,3 or 5 days Plasmapheresis, steroids and / or immun-supressive drugs are alternatives of IVIG if it’s ineffective.