POSTINFECTIOUPOSTINFECTIOUS S

NEUROPATHIESNEUROPATHIES

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

POLIOVIRUSES Virus (orally)

tonsilla Peyer

/ cervical lymph nods throat / mesenteric feces

\ secretions lymph nodes (1-6wk)

\ /

BLOOD STREAM

/ \ CNS Lymph nodes brown fat tissue

POLIOVIRUSESClinical manifestations1) Inapparent infection: Causes no disease, no sequela2) 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.