2.  Guillain-Barré syndrome (GBS) is an acute, frequently
severe, and fulminant polyradiculoneuropathy that is
autoimmune in nature.
 Males are at slightly higher risk for GBS than females,
and in Western countries adults are more frequently
affected than children.

3. Subtypes

4. Antecedent events
 Approximately 70% of cases of GBS occur 1–3 weeks after an
acute infectious process, usually respiratory or
gastrointestinal.
 Viruses e.g human herpes virus infection, CMV, Epstein-
Barr virus and Mycoplasma pneumoniae;
 Infection or reinfection with Campylobacter jejuni , recent
immunizations.
 The swine influenza vaccine, administered widely in the
United States in 1976, is the most notable example.
 Older-type rabies vaccine, prepared in nervous system
tissue, the mechanism is presumably immunization against
neural antigens.

5.  GBS occurs more frequently in patients with
 lymphoma (including Hodgkin's disease),
 HIV-seropositive individuals,
 Patients with systemic lupus erythematosus.
 C. jejuni has been implicated in summer outbreaks of
AMAN among children and young adults exposed to
chickens in rural China.

7.  Panel A shows the immunopathogenesis of acute
inflammatory demyelinating polyneuropathy.
 Autoantigens unequivocally identified, autoantibodies
bind to myelin antigens and activate complement.
 Formation of membrane- attack complex (MAC) on
the outer surface of Schwann cells and the initiation of
vesicular degeneration.
 Macrophages subsequently invade myelin and act as
scavengers to remove myelin debris.

8.  Panel B shows the immunopathogenesis of acute
motor axonal neuropathy.
 Myelinated axons are divided into four functional
regions: the nodes of Ranvier, paranodes,
juxtaparanodes, and internodes.
 Gangliosides GM1 and GD1a are strongly expressed at
the nodes of Ranvier, where the voltage-gated sodium
(Nav) channels are localized.
 Contactin associated protein (Caspr) and voltage-
gated potassium (Kv) channels are respectively present
at the paranodes and juxtaparanodes.

9.  IgG anti-GM1 or anti-GD1a autoantibodies bind to the
nodal axolemma, leading to MAC formation.
 Results in the disappearance of Nav clusters and the
detachment of paranodal myelin, which can lead to
nerve-conduction failure and muscle weakness.
 Axonal degeneration may follow at a later stage.
 Macrophages subsequently invade from the nodes into
the periaxonal space, scavenging the injured axons.

10. Neuropathies

12. Gangliosides

13.  Gangliosides, which are composed of a ceramide
attached to one or more sugars (hexoses) and contain
sialic acid (N-acetylneuraminic acid) are important
components of the peripheral nerves.
 Four gangliosides GM1, GD1a, GT1a, and GQ1b — differ
with regard to the number and position of their sialic
acids, where M, D, T, and Q represent mono-, di-, tri-,
and quadri-sialosyl groups.

14.  IgG autoantibodies to GM1 and GD1a are associated with
acute motor axonal neuropathy and its subtypes;
 Subtypes
 More extensive acute motor-sensory axonal neuropathy
 Less extensive acute motor conduction-block neuropathy,
not with acute inflammatory demyelinating
polyneuropathy.
 Motor and sensory nerves express similar quantities of GM1
and GD1a, but their expression within various tissues may
differ.
 This explains the preferential motor axon injury seen in
acute motor axonal neuropathy

15.  IgG autoantibodies to GQ1b, which cross-react with
GT1a, are strongly associated with the Miller Fisher
syndrome.
 Patients with pharyngeal–cervical–brachial weakness
 More likely to have IgG anti-GT1a antibodies, which
may cross-react with GQ1b,
 Less likely to have IgG anti-GD1a antibodies, which
suggests a link to the axonal Guillain–Barré syndrome
 Glossopharyngeal and vagus nerves strongly express
GT1a and GQ1b, possibly accounting for dysphagia in
this subtype.

17.  Guillain-Barré syndrome (GBS), Miller Fisher syndrome (FS) and
Bickerstaff brainstem encephalitis represent a spectrum of acute
post-infectious immune-mediated diseases.
 Miller Fisher syndrome (MFS) is characterized by an acute onset
of ataxia, areflexia without weakness and ophthalmoplegia.
 Miller Fisher syndrome (MFS) can be broadly categorized in to
two part,
 More extensive form, Bickerstaff brainstem encephalitis (BBE)
characterized by Miller Fisher syndrome with impairment of
consciousness

18.  Incomplete form
 Acute ophthalmoparesis without ataxia
 Acute onset ataxia neuropathy without
ophthalmoplegia
 Anti-GQ1b antibody syndrome includes
 Miller Fisher syndrome,
 Acute ophthalmoparesis, without ataxia
 Acute ataxic neuropathy, without ophthalmoplegia
 Bickerstaff’s brain-stem encephalitis
 Pharyngeal–cervical–brachial weakness.

19.  Anti-GQ1b IgG antibodies are found in >90% of patients
with MFS and titers of IgG are highest early in the course.
 GQ1b is strongly expressed in the oculomotor, trochlear,
and abducens nerves, and muscle spindles in the limbs.
 EO motor nerves are enriched in GQ1b gangliosides in
comparison to limb nerves.
 Pharyngeal–cervical–brachial weakness categorized as
localized form of acute motor axonal neuropathy or an
extensive form of the Miller Fisher syndrome.
 Half of patients of pharyngeal–cervical–brachial weakness
have IgG anti-GT1a antibodies, which often cross-react with
GQ1b.

20. Clinical symptoms
 Rapidly evolving hypo to areflexic motor paralysis with
or without sensory disturbance.
 Although hyporeflexia or areflexia is a hallmark of the
GBS, 10% of patients have normal or brisk reflexes
during the course of illness.
 Ascending paralysis, noticed as rubbery legs.
 The legs are usually more affected than the arms.
 Facial diparesis is present in 50% of affected
individuals.

21.  The lower cranial nerves frequently involved, causing
bulbar weakness.
 Mistaken for brainstem ischemia.
 Bladder dysfunction may occur in severe cases but is
usually transient.
 Autonomic involvement is common
 Loss of vasomotor control with wide fluctuation in
blood pressure, postural hypotension, and cardiac
dysrhythmias.

22.  Fever and constitutional symptoms are absent
 Deep tendon reflexes attenuate or disappear within
the first few days of onset
 Functions subserved by large sensory fibers, such as
deep tendon reflexes and proprioception, are affected.

23. Diagnostic criteria

25. GBS disability score
 0, A healthy state;
 1, Minor symptoms and capable of running;
 2, Able to walk 10 meters or more without assistance
but unable to run;
 3, Able to walk 10 meters across an open space with
help;
 4, Bedridden or chair bound;
 5, Requiring assisted ventilation for at least part of the
day;
 6, Dead.

26. Criteria for mechanical ventilation
in absence of clinical respiratory
distress
 Major
 Hypercarbia (partial pressure > 48 mm hg)
 Hypoxemia (partial pressure <56 mm hg)
 Vital capacity less than 15ml/kg body weight
 Minor
 Inefficient cough
 Impaired swallowing
 Atelectasis
1 major and 2 minor criteria needed

27. Brain 1996, 119,2053-2061
The prognosis and main prognostic indicators of GBS
 The percentage of patients with respiratoty failure
seemed to increase with age (<35 years,7%; 35-54 years,
13%; 55+ years, 18%)
 Mean age to clinical recovery was 157 days in patients
aged 35-54 years, and 253 days in patients 55 years and
older.
 Patients in whom gastroenteritis preceded the onset of
symptoms had the longest interval to clinical recovery.

28. DIFFERENTIAL DIAGNOSIS
 1.ACUTE POLYNEUROPATHIES
 Hepatic porphyria
 Critical illness polyneuropathy
 Diptheria
 Vasculitis
 Toxins -
arsenic,thallium,organophosphorus,lead,neurotoxic
fish

29.  DISORDER OF NEUROMUSCULAR JUNCTION
 Botulism
 Myaesthenia gravis
 Tick paralysis

30. POLYRADICULOPATHIES
 Inflammatory or neoplastic meningoradiculopthy
 Lyme radiculitis
 Cytomegalovirus lumbosacral radiculomyelopathy

31.  CNS DISORDERS
 Transverse myelitis
 Basilar artery thrombosis
 Rabies

32. MYOPATHEIS
 Hypokalemia
 Hypophosphatemia
 Rhabdomyolysis
 Polymyositis
 Critical care neuropathy

33.  ANTERIOR HORN SYNDROME
 Poliomyelitis
 West nile and enterovirus poliomyelitis

34. Paralytic Polio GBS
Fever occurs just Fever Occurs 2-3 weeks
before onset of before onset of
paralysis. paralysis
Asymmetrical Symmetrical
Descending Ascending
CSF-Normal Protein CSF-Increased
WBC 20- 300 proteins
WBC < 10

35. GBS vs BOTULINISM
 Bilateral symmetrical & descending flaccid paralysis occurs
after 12-36 hr of ingestion
 Oculobulbar weakness is an early feature of botulism.
Absence indicates an alternative diagnosis.(BMJ /best
practice)
 Nausea, vomiting, constipation, diplopia, ophthalmoplegia,
ptosis, blurring of vision, dysphagia, dysarthria, urinary
retention.
 There is No fever.
 Consciousness is not impaired
 Deep Tendon reflexes are absent.
 There is No sensory loss.
 CSF examination is normal.

36. Hypokalaemic periodic paralysis
 Symptoms typically begin in the first or
 second decade, attacks of flaccid paralysis usually
occurring on awakening in the night or in the early
morning. Weakness may be focal or generalized,
usually sparing facial and respiratory muscles, and
lasting for hours (occasionally days) with gradual
resolution.

37. THALLIUM POISONING
Ascending type of painful sensorimotor
neuropathy with abdominal pain, nausea
and vomiting(DTR can be present or
reduced)
Development of skin lesions on 10-15 th day
Hair loss between 15th to 20th day

38. GBS VS PORPHYRIA
 Abdominal pain, peripheral neuropathy, and changes
in mental status are the classic triad of an acute attack.
 Severe abdominal pain is the most commonly reported
presenting symptom during acute attacks.

40. GBS VS CRITICAL ILLNESS
POLYNEUROPATHY
 The neuromuscular syndrome of acute limb and
respiratory weakness that commonly accompanies
patients with multi-organ failure and sepsis
constitutes critical illness polyneuropathy.
 Vijayan J, Alexander M. Critical illness neuropathy.
Indian J Crit Care Med 2005;9:32-4

41. Vasculitic neuropathy
 systemic vasculitis/nonsystemic vasculitic neuropathy
 mononeuritis multiplex or asymmetric sensorimotor
neuropathy.
 Symmetric neuropathy is rare
 Asymmetric or multifocal painful sensorimotor
neuropathy is the most common presentation
 systemic symptoms (e.g.,unexplained weight loss,
fevers, rash); multiorgan involvement (e.g., joints,
skin, kidney, respiratory tract).

42.  INVESTIGATION –
 ELECTRODIAGNOSTIC STUDIES(NCS)
 CSF EXAMINATION

43. NERVE CONDUCTION
STUDIES

44.  CMAP amplitude
 NCV
 distal motor latencies (DML)
 F-wave latency
 H reflex
 Abnormal temporal dispersion
 Conduction block

45. CMAP
 The CMAP is the sum of all the action potentials
occurring individually in the contracting muscle
fibers.
 Motor nerve conduction is evaluated by recording the
compound muscle action potential (CMAP) associated
with a mechanical contraction of a given muscle
(twitch), in response to electrical stimulation of the
motor nerve fibers supplying that muscle.

46. CMAP Amplitude and Latency

47.  Why is it necessary to use two stimulation sites?
 The time between the shock and the appearance of the
CMAP (the latency) comprises three components:
 (1) time for action potentials to travel down the nerve,
 (2) time to cross the neuromuscular junction,
 (3) time for muscle action potentials to disperse throughout
the muscle.
 Only the first component is relevant to calculating nerve
conduction velocity. Including components (2) and (3)
would introduce a small systematic error, but these are
constants, and can be removed by subtracting the distal
stimulation site latency from the proximal site latency.

49. NERVE CONDUCTION VELOCITY

50. In a typical F wave study, a strong electrical stimulus
(supramaximal stimulation) is applied to the skin surface above the
distal portion of a nerve so that the impulse travels both distally
(towards the muscle fiber) and proximally (back to the motor
neurons of the spinal cord) as shown in figure.

51.  When the orthodromic stimulus reaches the muscle fiber, it
elicits a strong M wave indicative of muscle contraction.
When the antidromic stimulus reaches the motor neuron
cell bodies, a small portion of the motor neurons backfire
and orthodromic wave travels back down the nerve towards
the muscle.
 This reflected stimulus evokes small proportion of the
muscle fibers causing a small,second CMAP called the F
wave.
 The name F wave is derived since test was done the first
time in the intrinsic muscles of foot by Magladery and
McDougal in 1950. The afferent and efferent for F wave s are
alpha motor neurons.

53.  Why are F waves useful?
 F waves allow testing of proximal segments of nerves that
would otherwise be inaccessible to routine nerve
conduction studies. F waves test long lengths of nerves
whereas motor studies test shorter segments. Therefore F
wave abnormalities can be a sensitive indicator of
peripheral nerve pathology, particularly if sited proximally.
The F wave ratio which compares the conduction in the
proximal half of the total pathway with the distal may be
used to determine the site of conduction slowing—for
example, to distinguish a root lesion from a patient with a
distal generalised neuropathy

54. H REFLEX

55.  Hoffmann reflex (H-reflex) and muscle response (M-wave)
pathways. When a short-duration, low-intensity electric
stimulus is delivered, action potentials are elicited
selectively in sensory Ia afferents due to their large axon
diameter . These action potentials travel to the spinal cord,
where they give rise to excitatory postsynaptic potentials,
in turn eliciting action potentials, which travel down the
alpha motor neuron (αMN) axons toward the muscle
(response 3). Subsequently, the volley of efferent action
potentials is recorded in the muscle as an H-reflex.
Gradually increasing the stimulus intensity causes action
potentials to occur in the thinner axons of the αMNs
(response 1), traveling directly toward the muscle and
recorded as the M-wave

56. Conduction blocks
 Conduction block: compound musle action potential
amplitudes drop by more the 40% on proximal
stimulation compared to distal stimulation. Highly
suggestive of acquired demyelinating neuropathy.

57. Temporal dispersion (TD)
 Decrement-a reduction of the compound muscle
action potential (CMAP) on proximal versus distal
stimulation
 Abnormal decrement can also be the result of
increased temporal dispersion (TD), which is an
increase in the difference between the conduction
times along the different axons within a nerve.

58. Difference between demyelination
and axonal degeneration
 Demyelinating Neuropathy
 slow conduction velocity, prolonged sensory and
motor latencies, generally preserved amplitueds
 Axonal Neuropathy
 reduced sensory and motor amplitudes, normal
latencies and velocities, fibrillations and positive sharp
waves

59. Electrodiagnostic Medicine Criteria for
Peripheral Nerve Demyelination
 Conduction velocity reduced in 2 or more nerves
 1. If CMAP amplitude is > 80% of lower limit of normal
(LLN), the NCV must be < 80% of LLN.
 2. If CMAP amplitude < 80% of LLN, the NCV must be
< 70% of LLN

60. CMAP conduction block or abnormal temporal dispersion in
1 or more nerves
1. Regions to examine:
• Peroneal nerve between fibular head and ankle
• Median nerve between wrist and elbow
• Ulnar nerve between wrist and below elbow
2. Partial conduction block criteria
• CMAP duration difference between the above noted proximal
and distal sites of stimulation must be < 15%; and A > 20% drop in
CMAP negative spike duration, or baselineto- peak amplitude.
3. Abnormal temporal dispersion and possible conduction block
• CMAP duration difference between the above proximal and
distal sites of stimulation is > 15%; and
• > 20% drop in CMAP negative spike duration or baseline-topeak
amplitude.

61.  Prolonged distal motor latencies (DML) in 2 or
more nerves
 1. If CMAP amplitude is > 80% of LLN, the DML must
be > 125% of the upper limit of normal (ULN).
 2. If the CMAP is < 80% of LLN, the DML must be >
150% of ULN.
 Prolonged minimum F-wave latency or absent F-
wave
 1. F-waves performed in 2 or more nerves (10–15 trials)
 2. If the CMAP amplitude is > 80% of LLN, the F-wave
latency must be > 120% of ULN.
 3. If CMAP amplitude is < 80% of LLN, the F-wave
latency must be > 150% of ULN.

62. Salient features of NCS in GBS
 The most common EDX abnormalities seen in the first 2
weeks of illness are absent H reflex and absent,delayed or
impersitent F waves,finding that are common in
polyneuropathies but not specific for demyelinating type.
 Reduced CMAP amplitude or SNAPs in upper extremity
combined with normal Sural SNAPs (sural sparing) are
changes highly specific for diagnosis of AIDP and occurs in
50% of patient in first 2 weeks of illness
 Sural sparing combined with abnormal F waves has very
high sensitivity but occurs in only a third of patients during
first 2 weeks of illness.

63.  Conduction block of motor axons-recognised as
decrease of greater than 50% in CMAP amplitude from
distal to proximal stimulation in the absence of
temporal dispersion.
 Conduction block is highly specific for demyelination
but occurs in only 15-30% of early GBS.

64. CSF EXAMINATION
 Classic finding is elevated CSF protein with normal
cell count (albumino cytological dissociation). Occurs
in up to 90% at week 1 after symptom onset. CSF
protein is usually normal within the first 2 to 3 days
but then begins to rise very quickly, reaching a peak at
4 to 6 weeks and then persisting at a variably elevated
level for many weeks.

65.  CSF protein level varies from 0.45 to 3.0 g/L (45-300
mg/dL), but levels as high as 10 g/L (1000 mg/dL) can
be seen. Around 59% of patients with Bickerstaff
brainstem encephalitis (BBE) have elevated protein in
CSF

66.  Around 10% will not have a protein elevation and this
includes patients with the Miller-Fisher variant.
 Cell counts are typically <5 cells/mm^3. However, in
10% of patients, lymphocytosis <50 cells/mm^3 may
be present early on but quickly normalises over a few
days.

67.  HIV testing is done in high-risk person or presence of
CSF lymphocytic pleocytosis (>100 cell/mm^3)

68.  Monitoring of cardiac and pulmonary
dysfunction
 Electrocardiography, blood pressure, pulse
oximetry for oxyhemoglobin saturation, vital
capacity, and swallowing should be regularly
monitored in patients who have severe disease,
with checks every 2–4 hr if the disease is
progressing and every 6–12 hr if it is stable.
 Insertion of a temporary cardiac pacemaker, use
of a mechanical ventilator,and placement of a
nasogastric tube should be performed on the
basis of the monitoring results.
Guillain–Barré Syndrome. Nobuhiro Yuki, M.D., Ph.D., and Hans-Peter Hartung, M.D.. N
Engl J Med 2012; 366:2294-2304

69.  Prevention of pulmonary embolism
 Prophylactic use of subcutaneous heparin and
compression stockings is recommended for adult
patients who cannot walk.

70.  Immunotherapy
 Intravenous immune globulin or plasma exchange should be
administered in patients who are not able to walk unaided.
 In patients whose status deteriorates after initial
improvement or stabilization, retreatment with either form
of immunotherapy can be considered.
 However, plasma exchange should not be performed in
patients already treated with immune globulin because it
would wash out the immune globulin still present in the
blood. Also, immune globulin should not be used in patients
already treated with plasma exchange because this sequence
of treatments is not significantly better than plasma
exchange alone

71. Treatment
 A multidisciplinary consensus group has
recommended subcutaneous heparin and
graduated stockings to prevent deep
venous thrombosis and pulmonary emboli
in pt admitted in ICU.
 Hughes RA, Wijdicks EF, Benson E, Cornblath DR, Hahn AF,Meythaler JM, et al,
Multidisciplinary Consensus Group. Supportive care for patients with Guillain-Barré
syndrome. Arch Neurol 2005;62:1194-8.

72.  Recommendation: ACP recommends against the use of
mechanical prophylaxis with graduated compression
stockings for prevention of venous thromboembolism
(Grade: strong recommendation,moderate-quality
evidence).
 Recommendation: ACP recommends pharmacologic
prophylaxis with heparin or a related drug for venous
thromboembolism in medical (including stroke) patients
unless the assessed risk for bleeding outweighs the likely
benefits (Grade: strong recommendation, moderate-
quality evidence).
 Venous Thromboembolism Prophylaxis in Hospitalized Patients: A Clinical Practice
Guideline From the American College of Physicians. Ann Intern Med. 2011;155:625-632.

73.  The use of enoxaparin plus elastic stockings with
graduated compression, as compared with elastic
stockings with graduated compression alone, was not
associated with a reduction in the rate of death from
any cause among hospitalized, acutely ill medical
patients.
 Kakkar AK, Cimminiell C, Goldhaber SZ, Parakh R, Wang C, Bergmann JF; LIFENOX
Investigators. Low-molecular-weight heparin and mortality in acutely ill medical
.
patients. N Engl J Med 2011;365:2463-72

74. PAIN MANAGEMENT
 Pain management is not easy, but
gabapentin and carbamazepine may
help. Narcotic analgesics may
occasionally be needed
 Hughes RA, Wijdicks EF, Benson E, Cornblath DR, Hahn AF, Meythaler JM, et al, Multidisciplinary
Consensus Group. Supportive care for patients with Guillain-Barré syndrome. Arch Neurol
2005;62:1194-8.

75. Mechanical ventilation in GBS
 The major criteria are
 hypercarbia (partial pressure of arterial carbon
dioxide, >6.4 kPa [48 mm Hg]),
 hypoxemia (<7.5 kPa [56 mm Hg]) {partial pressure of
arterial oxygen while the patient is breathing ambient
air}
 vital capacity less than 15 ml per kilogram of body
weight
 Burakgazi AZ, Höke A. Respiratory muscle weakness in peripheral neuropathies. J
Peripher Nerv Syst 2010;15:307-13.

76.  Minor criteria are
 Inefficient cough
 Impaired swallowing
 Atelectasis
 Even in the absence of clinical respiratory distress,
mechanical ventilation may be required in patients
with at least one major criterion or two minor criteria.

77.  Rapid disease progression,
 Bulbar dysfunction,
 Bilateral facial weakness,
 Dysautonomia.
 Respiratory failure included vital capacity of less than 20 ml/kg,
 Maximal inspiratory pressure less than 30 cm H2O,
 Maximal expiratory pressure less than 40 cm H2O
 Reduction of more than 30% in vital capacity, maximal inspiratory
pressure, or maximal expiratory pressure.
 No clinical features predicted the pattern of respiratory decline;
however, serial measurements of pulmonary function tests allowed
detection of those at risk for respiratory failure.
 Lawn ND, Fletcher DD, Henderson RD, Wolter TD, Wijdicks EM. Anticipating Mechanical Ventilation in Guillain-
Barré Syndrome. Arch Neurol. 2001;58(6):893-898

78. Independent predictors of mechanical ventilation
Paul BS, Bhatia R, Prasad K, Padma MV, Tripathi M, Singh MB. Clinical predictors
of mechanical ventilation in Guillain-Barré syndrome. Neurol India 2012;60:150-3

79. PLASMA EXCHANGE
 Cochrane review has shown that plasma exchange is
better than supportive treatment .

80.  In five randomised but unblinded clinical trials of 623
patients, plasma exchange reduced the proportion of
patients needing ventilation from 27% to 14% (relative
risk 0.53, 95% confidence interval 0.39 to 0.74,
P=0.001). Similarly, the time taken to recover walking
with an aid was significantly shortened in two trials
(30 v 44 days, P<0.01).

81.  Therapeutic plasma exchange has been recommended
for moderate to severe weakness(defined as ability to
walk only with support or worse).
 French cooperative group on plasma exchange(1997)-
Even mildly affected patients benefit from two exchanges.
 Four exchanges were optimal for moderate to severe
cases and six exchanges did not have any additional
benefit.
 The recommended schedule entails a series of 4-5
exchanges(40-50 ml/kg) with a continuous flow
machine on alternate days, using saline and albumin as
replacement fluid.

82. PLASMA EXCHANGE
 Complications –
 Hematoma formation at puncture sites
 Pneumothorax after insertion of central line
 Catheter related septicemia

 Contraindications
 Septicemia
 Active bleeding
 Severe cardiovascular instability

83. IV IMMUNOGLOBULIN
 Although intravenous immunoglobulin has not been
tested against supportive treatment alone, a Cochrane
analysis of three trials indicated that such treatment
was equivalent to plasma exchange.

84.  Two of these trials were combined in a
meta-analysis of 398 patients, and change
of disability , time to walk unaided, and
proportion of patients unable to walk at
one year were not significantly different
between the two groups.
 Since these trials, intravenous
immunoglobulin has become the standard
treatment for the syndrome because it can
be given rapidly and has fewer side effects
than plasma exchange

85.  The standard regimen of 0.4 g/kg body weight each
day for five consecutive days is well tolerated.
 This dose is set empiricaly based on clinical experience
in patients with idiopathic thrombocytopenic purpura
 The combination of PE followed by IVIG was not
significantly better than PE or IVIG alone
 Six daily infusion of 0.4g/kg were reported to be
superior to three daily infusions in patients.(raphael et
al., 2001)

86. Monitor bulbar function, BP, fvc q2-6 hr FVC <12-15
Asses clinical severity ml/kg
Walks Walks with support or Mechanical
unassisted bedbound ventilation
No
progression Symptoms <14
days
Conservative
management
Plasma
IVIG exchange
Bradley’s neurology in clinical practice

87.  In vast majority of the patients with GBS treatment shoul
be initiated as soon as possible. Each day counts:<2 weeks
after the first motor symptoms.
 If the patient has reached plateau stage then treatment
probably is no longer indicated, unless the patient has
severe motor weakness and one cannot exclude the
possibility that an immunological attack is going on.
 (motor weak ness rapidly progresses initially but cease by 4
weeks. Nadir attained by 2 weeks in 50%,3 weeks in 80%
and 90% by 4 weeks)
 Harrison’s principles of internal medicine.

90. Side effects of iv ig
 Minor side effects
 Headache,myalgia,arthralgia,flulike symptom,
 Fever,vasomotor reaction
 Serious complication
 Anaphylaxis in lga defecient individuals
 Aseptic meningitis
 Congestive heart failure
 Thrombotic complication
 Transient renal failure

91. When plasma exchange is preferred over IVIG
 Hyperviscosity
 Congestive heart failure
 Chronic renal failure
 Congenital IGA defeciency

92. Corticosteroids for Guillain-Barré
syndrome
 Corticosteroids should not be used in the treatment of
GBS
 Hughes RAC, van der Meché FGA. Corticosteroids for Guillain-Barré
syndrome. The Cochrane Database of Systematic Reviews 2000,

94. PROGNOSIS OF GBS

95. Guillain-Barre´ Syndrome
Disability Score
0. HEALTHY STATE
1. MINOR SYMPTOMS AND CAPABLE OF RUNNING
2. ABLE TO WALK 10 M OR MORE WITHOUT ASSISTANCE BUT UNABLE TO RUN
3. ABLE TO WALK 10 M ACROSS AN OPEN SPACE WITH HELP
4. BEDRIDDEN OR CHAIRBOUND
5. REQUIRING ASSISTED VENTILATION FOR AT LEAST PART OF THE DAY
6. DEAD
Hughes RA, Newsom-Davis JM, Perkin GD, Pierce JM. Controlled trial prednisolone in acute
polyneuropathy. Lancet 1978;2:750–753

96. The Erasmus GBS outcome score
Age of onset >60 1
41-60 0.5
<40 0
Diarrhea Absent 0
present 1
GBS disability score 0 or 1 1
(at 2 weeks after entry) 2 2
3 3
4 4
5 5
EGOS 1-7

97.  If the EGOS is 3, the data suggest there is a <5%
chance the patient won’t be walking independently at
6 months;
 if EGOS is 4, the chance is 7%;
 if EGOS is 5, the chance is 25%;
 if EGOS is 6, the chance is 55%;
 and if EGOS is 7, the chance of not walking
independently at 6 months is 85%

98. Characteristics of included studies of intravenous immunoglobulin

99. Characteristics of included studies of plasma exchange

100. Characteristics of included studies of
corticosteroids

101. Jean Baptiste Octave Landry de Thézillat