1. POSTINFECTIOUS NEUROPATHIES

2. 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

5. 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

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

7. 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

8. 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!

9. 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.

10. 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

13. 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
cells/mm³ : PNL (early)  mononuclear.
CSF protein is normal or slightly elevated at the onset rises between mg/dl by the second week.

14. 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.

15. 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.

16. 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

17. 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.

18. 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.

19. 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.

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

21. 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

22. 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.