Guillain-Barré syndrome is a rare disorder where the immune system attacks the peripheral nervous system, causing muscle weakness and paralysis. It is usually preceded by a bacterial or viral infection. The main types are acute inflammatory demyelinating polyneuropathy, acute motor axonal neuropathy, and Miller Fisher syndrome. Clinical features include ascending paralysis and respiratory failure. Investigations include lumbar puncture, nerve conduction studies, and antibody testing. Treatment involves supportive care, plasmapheresis, IV immunoglobulins, and most patients recover fully, though some have persistent disability. Homeopathy treatments include Conium, Causticum, Lathyrus, and Natrum Mur depending on symptoms.

1. GUILLAIN-BARRÉ
SYNDROME
BY
DR PULLA UMA MAHESWARI
DEPARTMENT OF PAEDIATRICS
PG PART - II

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• DEFINE GBS
• EXPAIN THE PATHOPHYSIOLOGY OF GBS
• LIST THE TYPES OF GBS
• LIST THE CLINICAL FEATURES OF GBS
• DESCRIBE THE INVESTIGATIONS OF GBS
• EXPLAIN THE MNAGEMENT AND PROGNOSIS OF GBS
• EXPAIN THE HOMOEOPATHY MANAGEMENT
OBJECTIVES

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• Guillain Barre syndrome is a rare disorder in which body's
immune system attacks nerves and causes damage to the
peripheral nerves.
• The nerve injury often causes muscle weakness, cause
paralysis and sensitivity problems, including pain, tingling or
numbness.
DEFINITION

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• Acute idiopathic polyradiculoneuritis,
• Acute idiopathic polyneuritis,
• French polio,
• Landry's ascending paralysis
• Landry Guillain Barré syndrome
OTHER NAMES

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• Guillain-Barré is the result of a cell-mediated immune attack on peripheral nerve
myelin proteins.
• The best-accepted theory is that an infectious organism contains an amino acid that
mimics the peripheral nerve myelin protein.
• The immune system cannot distinguish between the two proteins and attacks and
destroys peripheral nerve myelin.
• The ganglioside GM1b, is the most likely target of the immune attack.
• With the autoimmune attack there is an influx of macrophages and other immune-
mediated agents that attack myelin, cause inflammation and destruction, and leave
the axon unable to support nerve conduction.
PATHO-PHYSIOLOGY

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AIDP ACUTE INFLAMMATORY DEMYELINATING
POLYRADICULONEUROPATHY
AMAN ACUTE MOTOR AXONAL NEUROPATHY
AMSAN ACUTE MOTOR AND SENSORY AXONAL NEUROPATHY
MFS MILLER FISHER SYNDROME
SUB-TYPES OF GB SYNDROME

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• It is the most common form and accounts for around 85– 90% of cases.
• The clinical features are of symmetrical ascending motor weakness with
hypo- or areflexia.
• The underlying pathological process involves inflammation and
destruction of the myelin sheaths surrounding peripheral nerve
axons by activated macrophages.
• This leads to slowing and blockage of conduction within peripheral nerves
causing muscle weakness.
• Severe cases may develop secondary axonal damage
AIDP

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• It is more common in Japan and China, amongst young people and in the
summer months.
• It has an association with precedent infection with Campylobacter jejuni.
• Clinical features are similar to AIDP but tendon reflexes may be preserved.
• Electrophysiological testing may distinguish from other variants as selective motor
nerve and axonal involvement is demonstrated.
• In AMAN the pathological process involves binding of antibodies to ganglioside
antigens on the axon cell membrane, macrophage invasion, inflammation and
axonal damage
AMAN

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• It is a variant of GBS in which both motor and sensory fibres are involved
and which can be demonstrated on electrophysiological studies.
• It is more severe and associated with prolonged or even partial recovery.
• Clinical features are similar to AMAN but also involve sensory
symptoms.
• The underlying pathological process is similar to that for AMAN (i.e.
antibody mediated axonal damage).
AMSAN

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• presents with ataxia, areflexia and ophthalmoplegia. 25% of patients may
develop limb weakness.
•Electrophysiological studies show primarily sensory conduction failure.
•Antiganglioside antibodies to GQ1b are found in 90% of patients and are
associated with ophthalmoplegia .
• There have been limited pathological studies in MFS but demyelination of
nerve roots has been demonstrated.
MFS

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• Hyporeflexia and weakness progress and may result in quadriplegia.
• Neuromuscular respiratory failure - demyelination of the nerves that innervate the
diaphragm and inter costal muscles results.
• Cranial Nerve deficit in (III- VII, IX- XII) with facial palsy.
• Ptosis, diplopia, facial weakness, dysarthria, dysphagia with pooling of secretions.
• Sensory dysfunction with abnormal proprioception, sensory ataxia can also occur.
• Difficult to speaking, chewing and swallowing, various muscles required to form
speech are weakened.
CLINICAL FEATURES OF GBS

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• Serum Biochemistry : Evidence of SIADH or Renal dysfunction.
• Inflammatory markers : Raised ESR and CRP sometimes
• Antiganglioside antibodies :
INVESTIGATIONS
Anti-GM1 It is positive in 25% of pts and is worse outcome
Anti-GD1a AMAN subtype of GBS
Anti-GQ1b Miller- Fisher syndrome

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• Infection screening : Campylobacter jejuni, Cytomegalovirus, Epstein-Barr virus, Herpes
simplex virus, Mycoplasma pneumoniae, HIV antibodies
• Radiological :
 A CT brain is indicated to exclude other causes of symptoms and evidence of raised
intracranial pressure prior to performing a lumbar puncture.
 An MRI of the spine may show selective anterior spinal nerve root enhancement with
gadolinium and will exclude cervical nerve impingement
• Nerve conduction studies
• Respiratory function tests:
– These may show reduced vital capacity, maximal inspiratory and expiratory pressures.
– Arterial blood gases may indicate progressive respiratory failure.

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• Lumbar puncture: Cell count and
glucose are usually normal with a
raised protein, although the latter may
also be normal in first two weeks.
• Electromyography: The electrodes
measure nerve activity in the muscles.

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• Supportive care
• Ventilatory support
• Plasmapheresis (plasma exchange)– to remove abnormal antibodies
• IV Immunoglobulin's – stop antibody damaging cells.
• Immunomodulatory intravenous immunoglobulin
– Muscle weakness
– Respiratory depression
MANAGEMENT

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• Most patients with GBS recover fully but this may take many months of
intensive therapy.
• 15% of patients suffer persistent disability. 10% are unable to walk
unaided at one year. There may be a recurrence in 2–5% of cases.
• The mortality from GBS ranges from 2–12%.
• Common causes of death include venous thromboembolism,
pneumonias, arrhythmias and complications related to dysautonomia.
PROGNOSIS

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 CONIUM : GB Syndrome with ascending paralysis
• There is trembling of lower limbs.
• Patient feels sudden loss of strength while walking along with painful
stiffness of the legs.
• Fingers of hands and toes feel numb.
HOMOEOPATHY MANAGEMENT

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 CAUSTICUM : GB Syndrome with gradually appearing paralysis
• There is progressive loss of muscular strength.
• Patient feels restlessness at night and sinking of strength.
• Muscles of forearm and hands remain unsteady.
• Numbness and loss of sensation are common.

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 LATHYRUS : GBS with rigidity of legs
• There is paralysis of the lower limbs.
• Spastic paralysis is common.
• Knees knock against each other while walking.
• The patient cannot extend or cross legs while sitting.
• Calf muscles remain tense.
• The toes do not leave the floor while the heel does not touch the floor.

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 VIPERA : GBS with increased reflexes
• This medicine is made from the poison of the viper snake and causes
paralysis similar to that of GBS.
• The patient feels obliged to keep his lower limbs raised.
• There is unbearable pain on letting the limbs hang down.

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 NATRUM MUR : GBS after fever
• The patient is anaemic, usually thin and withered.
• There is numbness and tingling in fingers and lower limbs.
• Hamstrings contract and cause pain.
• Heat and warmth aggravate the patient.
• There is increased thirst along with dryness of mouth.

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