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Gbs
1. Guillain-Barré syndrome (GBS)
Guillain-Barré syndrome (GBS) is an acquired immune-mediated inflammatory disorders of the peripheral nervous
system.
PATHOPHYSIOLOGY:
-The basis for flaccid paralysis and sensory disturbance is conduction block.Body’s response to the infection goes
awry and the immune system attacks the myelin and sometimes the axons of the peripheral nerves. As a result,
neurological signals are slowed, altered or blocked.
-Secondary axonal degeneration usually occurs. When a severe primary axonal pattern is encountered
electrophysiologically, the implication is that axons have degenerated and become disconnected from their targets,
specifically the neuromuscular junctions, and must therefore regenerate for recovery to take place.
Subtypes of Guillain-Barré Syndrome (GBS)
SUBTYPE
Acute inflammatory
demyelinating
polyneuropathy
(AIDP)
FEATURES
Adults affected more
than children; 90% of
cases in western
world; recovery rapid;
anti-GM1 antibodies
(<50%)
ELECTRODIAGNOSIS
Demyelinating
Acute motor axonal
neuropathy (AMAN)
Children and young
adults; prevalent in
China and Mexico; may
be seasonal; recovery
rapid; anti-GD1a
antibodies
Axonal
Acute motor sensory
axonal neuropathy
(AMSAN)
Mostly adults;
uncommon; recovery
slow, often
incomplete; closely
related to AMAN
Adults and children;
uncommon;
ophthalmoplegia,
ataxia, and areflexia;
anti-GQ1b antibodies
(90%)
Axonal
Miller Fisher
syndrome (MFS)
Axonal
PATHOLOGY
First attack on
Schwann cell surface;
widespread myelin
damage, macrophage
activation, and
lymphocytic
infiltration; variable
secondary axonal
damage
First attack at motor
nodes of Ranvier;
macrophage
activation, few
lymphocytes, frequent
periaxonal
macrophages; extent
of axonal damage
highly variable
Same as AMAN, but
also affects sensory
nerves and roots;
axonal damage usually
severe
Same as AMAN, but
also affects sensory
nerves and roots;
axonal
ETIOLOGY: unknown
- body's immune system begins to attack the body itself, causing what is known as an autoimmune disease.
-When GBS is preceded by a viral infection, there is no evidence of direct viral infection of peripheral nerves or
nerve roots.
INCIDENCE:GBS is the most frequent acquired demyelinating neuropathy, with an incidence of 0.6 to 1.9 cases per
100,000 population. The incidence increases gradually with age, but the disease may occur at any age. Men and
women are affected equally. The incidence increases in patients with Hodgkin disease, as well as with
pregnancy or general surgery.
2. Infections that may trigger GBS include:
Campylobacter jejuni, which can cause a type of food poisoning.
Mycoplasma , which can cause pneumonia.
Cytomegalovirus (CMV), which can cause fever, chills, sore throat, swollen glands, body aches, and fatigue.
Epstein-Barr virus (EBV), which can cause mononucleosis.
Varicella-zoster virus, which can cause chickenpox and shingles.
CLINICAL MANIFESTATION
-Appears days to weeks after symptoms of a viral upper respiratory or gastrointestinal infection.
- symmetriclimb weakness, often with paresthesia
- facialdiplegia, and dysphagia and dysarthria
- Tendon reflexes are lost
- degree of sensory impairment varies
- papilledema, sensory ataxia, transient extensor plantar responses, or evidence of autonomic dysfunction
(orthostatic hypotension, transient hypertension, or cardiac arrhythmia)
-muscle tenderness, and the nerves may be sensitive to pressure
DIAGNOSIS:
Rapid onset of ascending paralysis, rapid onset of sensory loss, marked hyporeflexia or areflexia, slowed nerve
conduction, absence of peripheral nerve lesion presentation
DIFFERENTIAL DIAGNOSIS:
diphtheritic polyneuropathy, acute anterior poliomyelitis, Porphyric neuropathy, Periodic paralysis
TREATMENT:
Medical:
Early plasmapheresis
IVIG therapy
Others:
Blood thinners may be used to prevent blood clots.
If the diaphragm is weak, breathing support or even a breathing tube and ventilator may be needed.
Pain is treated with anti-inflammatory medicines and narcotics, if needed.
Proper body positioning or a feeding tube may be used to prevent choking during feeding if the muscles
used for swallowing are weak.
PT MANAGEMENT:
Regular breathing exercises
Passive movements of all paralyzed limbs, to maintain full ROM
Positioning of Pillows and splinting e.g. ankles to prevent shortening of tendon ofachilles
PROM
Muscle strengthening & balancing exercises
Hydrotherapy
Gait training, reeducation
Ambulatory aids
