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