2. INTRODUCTION
Synonyms:
● AIDP: Acute Idiopathic demyelination
Polyneuropathy
● AIP: Acute Infective Polyneuropathy
● LGBSS: Landry Guillain Barre Strohl Syndrome
● AIP: Acute Idiopathic Polyneuropathy
● GBS Is defined as acute onset demyelinating
peripheral Polyneuropathy. It is ascending
Radiculopathy (always starts from lower limb to
upper limb), leads to flaccid paralysis.
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5. PREDISPOSING FACTORS
● Age: Common between 15 to 25 years of age.
● Gender: Common in Females.
● Infection: Viral in the form of Epstein Barr virus,
Bacteria in the form of mycoplasma pneumonia
● Vaccination: Rabies, typhoid, tetanus or Influenza
vaccination may precipitate the attack of GBS
● Surgery: After 4-5 weeks of major surgery patient
may shows signs of GBS which cab be attributed to
the following reasons: Due to surgical stress &
because of blood transfusion.
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● Drugs: Prolong use of antidepressant drugs like Zimelidine or gold
therapy which are neurotoxins are found to cause GBS
● Idiopathic: Without any known causes.
7. CLINICAL FEATURES
● The onset of GBS is acute or subacute
● Progression: The motor paralysis spreads
usually within 30 minutes to 4 weeks time. It
may take on an average 4 to 5 days for the
weakness to reach its peak. Once the
weakness reaches its peak it maintains a
plateau for 15-20 days following which the
patient recovers for 4-6 months. In rare cases
the recovery may extend upto 2 years also.
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● Motor: Weakness of the muscles which is of LMN type is seen with the
involvement of more than one limbs. The weakness is usually
symmetrical on both sides. The proximal parts are more involved than
distal parts although the disease may start from distal parts.
● Weakness of the facial & other cranial nerves may cause dysphagia,
diplopia & respiratory failure.
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● Sensory: Symptoms range from mild pain to
paresthesia. Total loss of sensation is usually not
seen.
● Myalgia or muscle pain occurs because of release of
a substance called cytokinin by the macrophages at
the Inflammatory foci of the nerve terminal.
● Sphincter disturbance: The patient may have
retention or overflow incontinence based upon the
involvement of sympathetic or parasympathetic
fibres supplying the urinary bladder.
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● Autonomic disturbance: Orthostatic hypotension is common in patient
with GBS due to lack of sympathetic mediated vascular response that
causes peripheral pooling of blood. Sweating may be totally lost or
profused.
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13. INVESTIGATION
● The albumin level in the CSF is increased
during the course of muscular weakness & it
may remain increased even for 4 weeks after
the muscular weakness has reached the
plateau.
● Electrophysiology shows an neurogenic type
of presentation with an increase in
amplitude, increase in the duration of the
motor unit potential with polyphasia.
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● DIABETIC NEUROPATHY
● About 15 percent of the patient with diabetes develop neuropathy
complication. Although not all will produce signs and symptoms. There
are different types of diabetic neuropathy which are as follows.
● Diabetic Mononeuropathy
● Only one or two nerves are involved. Most common cranial nerves
involved are third cranial nerves which causes weakness of the
extraocular muscles giving rise to diabetic ophthalmoplegia. The other
cranial nerves that can be frequently involved is sixth cranial nerve.
The peripheral nerves are not usually involved. Very rarely there is
involvement of either sciatic or femoral nerve. The exact mechanism of
neurogenic involvement is not known. However, it may be due to
involvement of the vascular supply to the nerves causing infarction.
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● Multiple Mononeuropathy
● This can be further divided into two types:
1. Rapidly evolving painful asymmetrical predominantly sensory
neuropathy.
2. Rapidly evolving painless asymmetrical predominantly motor
neuropathy.
● The first variety is very common in older age group with mild to
moderate neuropathy. The patients mainly has pain at the back which
may be radiating to the hip and even down to the thigh. The pain is
deep and aching in character and usually aggravates at night. Deep
tendon jerks may be involved at the knee mainly due to involvement of
the sensory pathway of the reflex arc. Motor symptoms are very rare
and are usually confined to hip and thigh musculature.
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● Unlike the above the second variety is predominantly motor
neuropathy causing gross weakness and wasting of the proximal
muscles at the hip, the thigh, and even involving the scapula and the
shoulder. Sensory symptoms are very rare and if present may manifest
as mild pain in the involved area. Reflexes may be reduced because of
the weakness of the muscles.
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● Thoracoabdominal Neuropathy
● In this type of neuropathy the patient has pain along one or
two segments of the thoracic spine. The pain may radiate
horizontally from the back to involve the abdominal area. EMG
studies have shown fibrillation potentials of the back muscles
and abdominal muscles confirming the involvement of spinal
nerve roots.
● The above type of neuropathies generally have a good
prognosis and faster recovery.
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● Distal Symmetric Neuropathy
● Most common type seen in diabetic patient. Usually begins with mild
sensory symptoms of pain or paresthesia which gradually spreads. The
sensory symptoms in the form of pain or paresthesia usually worsens at
night and are usually confined to the distal most part of the
extremities. Usually the altered sensation are present in the foot and
distal leg area and very rarely may also involve the hand and wrist.
This type of involvement of both the upper and lower limb has been
termed as “glove and stocking” appearance.
● In the later stages the patient may have involvement of the joints
causing arthropathy and may eventually cause charcot joints. Ankle
jerks are usually affected due to involvement of the sensory fibers of
reflex pathway
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● Autonomic Neuropathy
● Autonomic disturbances like pupillary and lacrimal dysfunction may be
noted in diabetic patients. There may be either increase or decrease of
sweating. The most common autonomic disturbance seen in diabetic
patient is postural hypotension which occur due to peripheral pooling
of blood. The exact cause of autonomic involvement is not properly
understood. However the following three mechanism have been put
forth.
● Accumulation of vacuoles and granules in sympathetic ganglia
● Demyelination of the nerve fibers
● Loss of cell in the intermediate lateral column in the spinal cord.