POLYNEUROPATHIES

SYEDA AFSHEEN
DPT/MSPT NEUROLOGICAL
POLYNEUROPATHIES

 Polyneuropathy affects several nerves in different parts

of the body at the same time. In cases of
mononeuropathy, just one nerve is affected.
 Polyneuropathy can affect nerves responsible for feeling
(sensory neuropathy), movement (motor neuropathy), or
both (sensorimotor neuropathy).
 Diabetes: This can be a significant risk factor, especially
if blood glucose levels are poorly controlled. One study
of more than 1,400 people with type 2 diabetes found
that every fifth person had diabetic neuropathy.
 Alcohol abuse: Alcohol can damage nerve tissue, and
alcohol abuse is often associated with nutritional
deficiencies that contribute to neuropathy.
 Autoimmune conditions: The immune system attacks
the body, causing damage to nerves and other areas.
Conditions include Sjogn's syndrome, receliac disease,
Guillain-Barré syndrome, rheumatoid arthritis, and lupus
.
 Bacterial or viral infections: Certain infections can lead
to neuropathy, including Lyme disease, shingles,
hepatitis B, hepatitis C, and HIV.
 Bone marrow disorders: Examples of these include
abnormal proteins in the blood, some forms of
bone cancer, and lymphoma.
 Exposure to toxins: Toxic neuropathy may be caused by
exposure to industrial chemicals such as arsenic, lead,
mercury, and thallium. Drug or chemical abuse is also a
risk factor.
 Hereditary disorders: Certain conditions, such as
Charcot-Mar
 ie-Tooth disease, are forms of hereditary neuropathy.

 Hypothyroidism: An underactive thyroid may lead to

polyneuropathy, although this is uncommon.
 Kidney disease: Uremic neuropathy is a form of
polyneuropathy that affects 20 percent to 50 percent of
people with kidney disease, according to the Center for
Peripheral Neuropathy.
 Medications: Chemotherapy, along with some drugs
used to treat HIV/AIDS, can cause neuropathy.
 Poor nutrition: Deficiencies of vitamins B-1, B-6, B-12,
and E may lead to polyneuropathy, as these are vital for
nerve health.
CONDITIONS ASSOCIATED WITH
POLYNEUROPATHY

Charcot-Marie-Tooth Disease
diabetes
diphtheria
Guillain-Barré Syndrome
hepatitis B
hepatitis C
HIV/AIDS
kidney disease
leprosy
liver disease
Lyme disease
lymphoma
osteosclerotic myeloma
pernicious anemia (vitamin B-12 deficiency)
radiculopathy
rheumatoid arthritis
shingles
TYPES

 There are more than 100 types of peripheral neuropathy,

and most of these are polyneuropathies.
 There are three main patterns of polyneuropathy:

 Chronic symmetrical peripheral neuropathy: Most

polyneuropathies are chronic and develop over
many months.
 Multiple mononeuropathy: There is damage to at least
two separate nerve areas.
 Acute symmetrical peripheral neuropathy: This is
rare. The most common cause is
Guillain-Barré syndrome, a condition that can be fatal.
GUILLAIN-BARRE SYNDROME
 Guillain-Barre (gee-YAH-buh-RAY) syndrome is a rare
disorder in which your body's immune system attacks
your nerves. Weakness and tingling in your extremities
are usually the first symptoms.
PATHOPHYSIOLOGY
•Usually post infectious
•Immune-mediated: infectious agents thought to
induce Ab production against specific
gangliosides/glycolipids
•Lymphocytic infiltration of spinal roots/peripheral
nerves & then macrophage-mediated, multifocal
stripping of myelin
•Result: defects in the propagation of electrical
nerve impulses, with eventual conduction block
and flaccid paralysis
CLINICAL FEATURES
 Progressive, fairly symmetric muscle weakness
 typically starts in proximal legs

 10% will 1st develop weakness in face or arms

 severe respiratpry muscle weakness in 10-30% pts

 oropharyngeal weakness in ~ 50%

CLINICAL FEATURES
• Prickling, pins and needles sensations in your fingers, toes,
ankles or wrists
• Weakness in your legs that spreads to your upper body
• Unsteady walking or inability to walk or climb stairs
• Difficulty with eye or facial movements, including speaking,
chewing or swallowing
• Severe pain that may feel achy or cramplike and may be worse
at night
• Difficulty with bladder control or bowel function
• Rapid heart rate
• Low or high blood pressure
• Difficulty breathing
RISK FACTORS
• Guillain-Barre syndrome may be triggered by:
• Mostcommonly, infection with campylobacter, a type of bacteria often
found in undercooked poultry
• Influenza virus
• Cytomegalovirus

• Epstein-Barr virus
• Zika virus
• Hepatitis A, B, C and E
• HIV, the virus that causes AIDS
• Mycoplasma pneumonia
• Surgery

• Hodgkin's lymphoma
• Rarely, influenza vaccinations or childhood vaccinations
DIAGNOSIS:
 Albuminocytologic dissociation: elevated CSF protein
w/ normal WBC (80-90% pts)
 Electromyography (EMG) helps confirm diagnosis =
prolonged or absent F waves
 GBS VARIANTS

 Think of AIDP as the traditional form as described

previously, accts for 85-90%
 Miller Fisher Syndrome: opthalmoplegia, ataxia, and
areflexia (5%). GQ1b antibody. Only 1/4th w/
extremity weakness
 AMAN: selective involvment of motor nerves, DTRs
are preserved, more common in Japan/China, almost
all preceded by Campylobacter infxn
 AMSAN: more severe form of AMAN +sensory
SUPPORTIVE CARE
 Monitor Resp status closely (follow NIFs), up to 30%
may req ventilatory support
 In severe cases, intrarterial monitoring may be necessary
given the gisngifcant blood pressure fluctuations
 Neuropathic pain plagues most, often managed w/
Gabapentin or Carbamazepine
DISEASE MODIFYING TREATMENT
•IVIG : typically given for 5 d at 0.4 gram/kg/d
(may need to extend course depending on
response)
•Plasmapheresis: usually 4-6 treatments over 8-10
days

The choice b/w plasma exchange and IVIG is dep

on availability, pt contraindications, etc. Because
of ease of administration, IVIG is frequently
preferred. The cost and efficacy of the 2
treatments are comparable.
Glucocorticoids have NO ROLE!!
OUTCOMES
 65% can walk independently @ 6 mos
 Overall, 80% usually recover completely

 5-10% have prolonged course w/ incomplete recovery,

~3% wheelchair bound
 Approx 5% die despite ICU care

 2% will develop chronic relapsing Chronic Inflammatory

Demyelinating Polyradiculoneuropathy (CIDP)
CHRONIC DEMYELINATING
POLYNEUROPATHY
 Chronic inflammatory demyelinating polyneuropathy
(CIDP) is a neurological disorder characterized by
progressive weakness and impaired sensory function in
the legs and arms.
 The disorder, which is sometimes called chronic
relapsing polyneuropathy, is caused by damage to the
myelin sheath (the fatty covering that wraps around and
protects nerve fibers) of the peripheral nerves.
 CIDP – CLINICAL FEATURE
• Initiallimb weakness, both proximal and distal
• Sensory symptoms (eg, tingling and numbness of hands and feet)

• Motor symptoms (usually predominant)

• In about 16% of patients, a relatively acute or subacute onset of

symptoms
• In children, usually a more precipitous onset of symptoms

• Symptoms of autonomic system dysfunction (eg, orthostatic

dizziness)Cmay branial nerves
CIDP – THERAPY

 Corticoids
 Immunosupresant – azathioprin, cyklophosfamid

 Plazmapheresis

 IVIg – 400 mg/kg/day 4-6 times

 Physiotherapy
PROGNOSIS
 The course of CIDP varies widely among individuals.
Some may have a bout of CIDP followed by spontaneous
recovery, while others may have many bouts with partial
recovery in between relapses.
 The disease is a treatable cause of acquired neuropathy
and initiation of early treatment to prevent loss of nerve
axons is recommended. However, some individuals are
left with some residual numbness or weakness.
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