POSTINFECTIOUS NEUROPATHIES POLIOVIRUSES w Member of enteroviruses Picornoviridae

POSTINFECTIOUS NEUROPATHIES

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

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

POLIOVIRUSES Virus (orally) tonsilla / Peyer cervical lymph nods throat / mesenteric feces secretions lymph nodes (1 -6 wk) / BLOOD STREAM / CNS Lymph nodes brown fat tissue

POLIOVIRUSES Clinical manifestations w 1) Inapparent infection: Causes no disease, no sequela w 2) Abortive PM: Brief febrile illness. Malaise, anorexia, nausea, vomiting, sore throat constipation, diffuse abdominal pain. w 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 w 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 w 4) Paralytic PM: Nonparalytic PM + waekness of one / more muscle group w These symptoms may be followed by a symptom free interval of several days and the recurrence of disease w Bladder paralysis lasting 1 -3 days occurs approximately 20 % of patients.

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

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

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

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

POLIOVIRUSES w Prevention vaccination IPV. w OPV – vaccine of choice in countries where polio is endemic. w 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 w Postinfectious polyneuropathy causes demyelination in mainly motor but sometimes also sensory nerves. w Affects people of all ages and not hereditary. Paralysis usually follows a nonspesific viral infection by abaut 10 days (camphylobacter jejuni, mycoplasma pneumoniae) w Weakness begins usually in the lower extremities and progressively involves the trunk, the upper limbs and finally bulbar muscles.

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

GUILLAIN-BARRE SYNDROME w Dysphagia and facial weakness are often impending signs of respiratory failure w Urinary incontinance or retention of urine is transient. w 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. w Lability of blood pressure and cardiac rate, postural hypotension , bradycardia.

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

GUILLAIN-BARRE SYNDROME w Diagnosis: CSF: protein is elevated to more than twice the upper limit of normal. w Glucose Normal w No pleocytosis w 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 w EMG: Evidence of acute denervation of muscle. w Serum CK: mildly elevated/N w Treatment: rapidly progressive ascending paralysis is treated with IVIG adm 2, 3 or 5 days w Plasmapheresis, steroids and / or immun -supressive drugs are alternatives of IVIG if it’s ineffective.