Transcript CPC - Scott & White Memorial Hospital

CPC: A Paralysis
Quandary for a Dime
Alan Trumbly, DO
Objectives
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Case Presentation
Problem List
Locate the Lesion
Develop Differential
Relate Differential to patient
Cross fingers and choose…
Patient
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CC: Progressive Upper Extremity Weakness.
HPI:
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70 y.o. Right handed, Hispanic Male.
2 weeks ago developed fever, chills, nausea, vomiting,
abdominal cramping, diarrhea. Symptoms resolved in 24-36
hours.
2 Days PTA: Left upper extremity numbness, tingling, and
weakness.
1Day PTA: Continued to progressively worsening, and by the
PM both upper extremities involved.
Transferred to S/W on day of admission for further
neurological workup.
Patient

HPI: On day of admission
Both arms quite weak.
 Dull aching neck pain, especially with rotation to the
right.
 NO diploplia, ptosis, dysarthria, dysphasia, shortness
of breath, lower extremity weakness, or bowel or
bladder incontinence.
 NO pain in limbs or back.
 NO prior neurological history, except lumbar
laminectomy for Left L4-L5 radiculopathy.
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Patient
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PMH:
Hypertension
 Hyperlipidemia
 Diabetes: good blood sugar control, no neuropathy.
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Fam Hx: negative for neurological disease.
Soc Hx: No tobacco or alcohol.
Allergies: none
Medications: none
Patient
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Vitals: Afebrile
PExam:
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Gen: pleasant, straightforward, Hispanic man, upset,
but no distress, alert and
oriented with no dysarthria.
CN: visual fields full, pupils
react 3 to 2 mm, no
papilledema, ocular motility
full, no nystagmus. Mild left
facial weakness. Masseter and
temporalis strength and bulk,
as well as pterygoid strength all
normal.
Patient
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PExam:
 Palate elevated briskly midline.
 Right deviation of the tongue with protrusion.
 Left SCM and Trapezius were weak.
 Right SCM and Trapezius were normal.
 Motor: no fasciculations or atrophy
 Upper ext: Deltoids 2/5 bilaterally, Triceps 4-/5 right, and
3/5 on the left. Finger and wrist extensors 0/5
 Reflexes: Absent in the upper extremities, , trace at the right
knee, absent at the ankles. Plantar responses were neutral
bilaterally.
Patient
Finger and wrist extentsors
0/5 bilaterally.
Interosseous muscles 2/5
bilaterally.
Hand Grips 3/5 bilaterally.
ABSENT in
upper
extremities
Triceps 4-/5 right, 3/5 left.
Deltoids 2/5 bilaterally
Quads 5/5
Right hip
flexor 4+/5
and left 5/5
Trace at right
knee
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Motor:
Reflexes:
ABSENT at
ankles
Foot Dorsiflexion:
4+/5 Right, and 4/5 left
Patient
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PExam:
All sensory modalities reported normal.
 Plantar responses neutral bilaterally.
 Gait: not testable.
 Cerebellar: not testable.
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Labs:
142 103 13
4.2
30
1.0
Tot Bili: 0.8
Alk Ph: 90
AST: 23
ALT: 32
Tot Prot: 7.0
Alb: 4.1
5.8
13.7
38.9
MCV: 84.4
208
Our Mission
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Additional studies were done upon arrival here
and a diagnosis was made???
Problem List
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Subacute (days) Progressive Upper Extremity Weakness
Absent Muscle Stretch Reflexes
Rightward deviation of the tongue, and Left SCM and
Trapezius were weak
Recent Diarrhea Illness (2 weeks prior)
Diabetes
Hypertension
Hx of Lumbar laminectomy
FDR
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32nd President
Presidency spanned the
Great Depression of
1930’s, and most of
World War II.
Only U.S. president to
have served more than
two terms.
Location, Location, Location
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What are symptoms to
look for?
What are the locations
possible?
Signs that Distinguish Patterns of
Weakness
Sign
UMN
LMN
Myopathic
Atrophy
None
Severe
Mild
Fasciculations
None
Common
None
Tone
Spastic
Decreased
Norm/Dec
Distribution
Pyramidal/regional
Distal/segmental
Proximal
DTR
Hyperactive
Hypoactive/absent
Normal/hypoactive
Babinski
Present
Absent
Absent
Location, Location, Location
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Hemisphere
Brainstem
Cerebellum
Cord
AHC
Root
Plexus
Nerve
NMJ
Muscle
Location, Location, Location
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Hemisphere
Brainstem
Cerebellum
Cord
AHC
Root
Plexus
Nerve
NMJ
Muscle
Location, Location, Location
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Hemisphere
Brainstem
Cerebellum
Cord
AHC
Root
Plexus
Nerve
NMJ
Muscle
Location, Location, Location
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Hemisphere
Brainstem
Cerebellum
Cord
AHC
Root
Plexus
Nerve
NMJ
Muscle
FDR
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Founded the National Foundation for Infantile
Paralysis in the US in 1938, which funded rehab
programs for victims of paralytic polio and the
development of the vaccine.
Now known as the March of Dimes.
Acute Weakness
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Spinal Cord Disease:
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Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:
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Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis
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NMJ disease:
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Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:
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Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Acute Weakness

Spinal Cord Disease:
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
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
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Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:
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

Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:
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Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Acute Weakness
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Spinal Cord Disease:
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
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


Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:



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
Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Acute Weakness
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Spinal Cord Disease:
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

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Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:





Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Acute Weakness
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Spinal Cord Disease:
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




Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:





Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Acute Weakness

Spinal Cord Disease:






Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:

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Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Myesthenia Gravis
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Young women and older men
Diplopia, Dysarthria, Dysphagia, Dyspnea
Deficits are fatigable.
Pure muscular weakness without the atrophy,
and normal DTR, Sensation, Mentation, and
Sphincter tone.
Lambert-Eaton Syndrome: Paraneoplastic,
DTR absent but improve with exercise,
incontinence present, and antibody mediated.
Acute Weakness
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Spinal Cord Disease:
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
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Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:





Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Botulism
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Abdominal and GI symptoms preceding
syndrome that resembles myasthenia gravis.
Improperly canned foods contaminated with the
exotoxin of Clostridium botulinum.
Rapidly developing paralysis usually affects the
ocular and cranial musculature first then
generalized (Descending).
Toxin-mediated inhibition of acetylcholine
release from axon terminals at NMJ.
Acute Weakness
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Spinal Cord Disease:
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
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


Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:





Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Organophosphate Poisoning
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Miosis, Excessive bodily secretions, and
fasciculations.
Decreased acetylcholinesterase activity that
causes excessive acetylcholine at the NMJ.
Symptoms vary 5 to 12 hours after exposure.
Tx with atropine.
Acute Weakness

Spinal Cord Disease:






Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:





Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
FDR
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August, 10 1921, FDR
was 39 y.o. fell into Bay
of Fundy, near
Campobello, New
Brunswick.
1933, elected President
of the US with
symmetrical lower
extremity weakness.
Acute Weakness
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Spinal Cord Disease:
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


Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:





Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Spinal Cord Disease
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Signs and symptoms occur at affected area and below.
Associated with UMN lesions.
Caused by compressive or noncompressive lesion.
Central Cord Syndrome:
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Most often caused by syringomyelia and intramedullary cord
tumors.
Pathological process starts centrally and proceeds
centrifugally, producing motor and sensory signs.
Suspended sensory loss: decussating spinothalamic tract fibers are
affected, loss of pain and temperature is bilateral, “cape
distribution”>>> “sacral sparring”.
Acute Weakness

Spinal Cord Disease:






Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:





Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Anterior Horn Cell Disease
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Cell bodies of peripheral motor nerves.
Amyotrophic Lateral Sclerosis:
Most common, affects AHC and corticospinal tracts.
 Distal bilateral weakness, with atrophy and
fasciculation's (LMN signs), combined with bulbar
signs, hyper-reflexia, upgoing toes (UMN signs).
 Asymmetric limb weakness.

Post-Polio Syndrome
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Major cause of morbidity and death throughout the
world during the first half of the 20th century.
Young children characterized by a mild, brief febrile
illness.
Small group would develop fever, HA, meningeal
irritation, soreness, and asymmetric paralysis.
Introduction of the inactivated polio vaccine in 1954.
West Nile Virus
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RNA flavivirus.
Majority asymptomatic, 20% develop febrile disease,
and only 1% will develop neuroinvasive disease (aseptic
meningitis, encephalitis, or flaccid paralysis).
Abrupt onset of fever, headache, myalgia, weakness,
and often, abdominal pain, nausea, vomiting, or
diarrhea.
Flaccid paralysis caused by WNV infection is similar
clinically and pathologically to poliomyelitis caused by
poliovirus, with damage of anterior horn cells.
Acute Weakness

Spinal Cord Disease:






Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:





Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Transverse Myelitis



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
Inflammatory diseases of the Spinal Cord: viral, bacterial,
fungal, parasitic, noninfectious.
Antecedent event that precede symptoms by days to 1-2 weeks.
Demyelinating and inflammatory process leading to an
incomplete cord lesion initially produce a flaccid areflexic
paralysis known as spinal shock, and acute UMN paralysis.
Marked disturbances in autonomic function can occur below the
level of the lesion.
All sensory modalities are lost below the level of the lesion.
Radicular pain is common at the level of the lesion.
Acute Weakness

Spinal Cord Disease:






Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:





Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Tick Paralysis






Rocky Mountain wood tick (Dermacentor andersoni) and the
American dog tick (Dermacentor varaibilis).
Symptoms within 2-7 days.
Bilateral Lower Extremity weakness that progresses to paralysis,
ascends upward to trunk, arms, and head within hours and may
lead to respiratory failure and death.
Minor sensory symptoms but constitutional signs are usually
absent.
DTR’s are usually hypoactive or absent and opthalmoplegia and
bulbar palsy can occur.
Human cases are rare and usually occur in children under the age
of 10.
Acute Weakness

Spinal Cord Disease:






Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:





Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Arsenic Poisoning





Symptoms: violent GI symptoms, sense of
dryness and tightness in the throat, thirst,
hoarseness, and difficulty of speech.
Emerald Green.
Arsenicosis - chronic arsenic poisoning from
drinking water, New Hampshire.
Check hair follicles.
Tx: Chelating agents.
Acute Weakness

Spinal Cord Disease:






Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:





Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Acute Intermittent Porphyria




Rare metabolic disorder in the production of heme.
Deficiency of the enzyme porphobilinogen
deamniase leads to the metabolite porphyrin
accumulating in the cytoplasm.
Symptoms of AIP may include abdominal pain,
constipation, and muscle weakness.
Look for trigger.
Acute Weakness

Spinal Cord Disease:






Transverse Myelitis
AHC Disease
Epidural and Extradural
Tumor or Spinal Cord tumor
Epidural Hematoma
Herniated intervertebral disk
Peripheral Nerve Disease:




Guillain-Barre’ Syndrome
Acute intermittent porphyria
Arsenic poisoning
Tick paralysis

NMJ disease:




Myasthenia gravis
Botulism
Organophosphate poisoning
Muscle disease:





Polymyositis
Rhabdomyolysis-myoglobinuria
Acute alcoholic myopathy
Electrolyte imbalances
Endocrine disease
Guillain-Barré Syndrome




1859, Landry’s ascending paralysis.
1916, Guillain and Barré described the CSF findings.
Acquired demyelinating disorders of the peripheral
nervous system with an acute onset.
Heterogeneous syndrome with several variants:



Acute inflammatory demyelinating polyradiculoneuropathy
(AIDP)
Miller-Fisher Syndrome
Acute axon loss ("axonal") polyradiculopathy



Acute motor axonal neuropathy
Acute motor-sensory axonal neuropathy
Other variants
GBS: Pathogenesis



Antecedent infection evokes an immune
response, this in turn cross-reacts with
peripheral nerve components. (Molecular
Mimicry)
Results in acute polyneuropathy as the response
in directed toward myelin or the axon of PN.
Rabbits sensitized with C. jejuni
lipooligosaccharide or GM1, would develop
anti-GM1 IgG antibodies and paralysis.
GBS: Clinical Features
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Usually begins distal legs, but 10% in arms or face.
50% will develop facial weakness and/or oropharygeal
weakness.
15% develop oculomotor weakness.
80% develop parasthesias, usually mild.
Often severe low back pain.
30% develop severe respiratory muscle weakness
requiring ventilatory support.
Dysautonomia in 70%: HR, BP, urinary retention, ileus,
loss of sweating, and occasionally Sudden Death.
GBS: Antecedent Events
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70% of cases or 2/3’s, 1-3 weeks prior.
Campylobacter jejuni: Most common, worse prognosis
HIV: any stage.
Other infections: CMV, EBV, Hepatitis, Mycoplasma
pneumoniae, Influenza, Herpes.
Vaccination: Influenza, Meningococcal (MCV4; report
to VAERS).
Small percentage: Surgery, Trauma, BM Transplant,
TNF-alpha antagonist, and systemic illnesses.
AIDP
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Most Common in US and Europe. 85-90% of
cases.
Peripheral nerve myelin is the target of immune
attack.
Typical clinical features: progressive, fairly
symmetric muscle weakness accompanied by
absent or depressed DTR.
Miller-Fisher syndrome
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5% of cases in US and 25% in Japan.
Ophthalmoplegia, ataxia, and areflexia. And
~1/3 will have some extremity weakness.
Associated with antibodies to ganglioside GQ1b
in 85-90%.
AMAN/AMSAN
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First recognized in 1986.
More frequent in China, Japan, and Mexico, but still 510% of GBS in US.
More severe course than demyelinating GBS; antibodies
to GM1 in some cases.
60-70% preceded by Campylobacter jejuni infection.
Seasonal incidence, being more frequent in the summer.
AMSAN: More severe form of AMAN, pathology is
predominantly axonal lesions of both motor and
sensory nerve fibers.
GBS: Lab features
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Albuminocytologic Dissociation: normal WBC
with an elevated CSF Protein level. 80-90% of
patients with GBS at one week after sx onset.
EMG and NCS: acute polyneuropathy with
predominate demylinating features in AIDP, and
axonal in AMAN and AMSAN.
Glycoprotein Antibodies: Anti GQ1b in 8590% of MFS.
GBS: Diagnostic Criteria
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Required features: Progressive weakness and Areflexia.
Supportive features include:
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Progression of symptoms over days to four weeks
Relative symmetry
Mild sensory symptoms or signs
Cranial nerve involvement, especially bilateral facial nerve weakness
Recovery starting two to four weeks after progression halts
Autonomic dysfunction
No fever at the onset
Elevated protein in CSF with a cell count <10 mm3
Electrodiagnostic abnormalities consistent with GBS
GBS doubtful:
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Sensory level
Marked, persistent asymmetry of weakness
Severe and persistent bowel and bladder dysfunction
More than 50 white cells in the CSF
Criteria for diagnosis of Guillain-Barre syndrome. Ann Neurol 1978; 3:565.
GBS: Treatment
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Supportive Care:
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Impending Respiratory Arrest: FVC <20 mL/kg, Maximum inspiratory
pressure <30 cmH2O, Maximum expiratory pressure <40 cmH2O.
Prospective study of 722 GBS patients, 313 req mechanical
ventilation.
Predictors of intubation:
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Time of onset to admission less than seven days
Inability to cough
Inability to stand
Inability to lift the elbows
Inability to lift the head
Liver enzyme increases
Sharshar T; et.al. Crit Care Med 2003 Jan;31(1):278-83.
GBS: Treatment
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Autonomic dysfunction: monitor BP, fluid
status, and cardiac rhythm. Monitor B/B
function.
Pain Control: 40-50% pts have neuropathic pain.
Plasma Exchange: remove circulating antibodies,
complement, and other agents.
IVIG : unknown, possibly anti-idiotypic
antibodies interfering with T and B cells.
GBS: Treatment
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AAN Observations:
Treatment with plasma exchange or IVIG hastens
recovery from GBS.
 The beneficial effects of plasma exchange and IVIG
are equivalent.
 Combining the two treatments is not beneficial.
 Steroid treatment alone is not beneficial.

Neurology 2003 Sep 23;61(6):736-40.
“What was the cause of FDR’s
paralytic illness?”

A.S. Goldman, et. al. Journal of Medical Biography 2003;
11:232-240.
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1) Protracted symmetric ascending paralysis over 10-13 days
2) Facial paralysis
3) Bladder and bowel dysfunction
4) Numbness and Dysaesthesia
5) Absence of meningismus
6) Descending pattern of recovery
7) Fever
8) Permanent paralysis
Disease incidence in age group x symptom probability.
Six of eight favored GBS.
J Med Biogr. 11: 232–240 (2003)
FINAL ANSWER
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
Perform LP, anti
GQ1b, EMG and
NCS.
GBS, possibly
AMAN variant.
References
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www.uptodate.com
Harrisons
Goetz: Textbook of Clinical Neurology, 2nd ed. Copyright © 2003 Saunders,
An Imprint of Elsevier.
Criteria for diagnosis of Guillain-Barre syndrome. Ann Neurol 1978; 3:565.
Early predictors of mechanical ventilation in Guillain-Barre syndrome.
Sharshar T; Chevret S; Bourdain F; Raphael. Crit Care Med 2003
Jan;31(1):278-83.
Practice parameter: immunotherapy for Guillain-Barre syndrome: report of
the Quality Standards Subcommittee of the American Academy of
Neurology. Hughes RA; Wijdicks EF; Barohn R; Benson E; Cornblath DR;
Hahn AF; Meythaler JM; Miller RG; Sladky JT; Stevens JC. Neurology 2003
Sep 23;61(6):736-40.
Goldman, AS et al, What was the cause of Franklin Delano Roosevelt's paralytic
illness?. J Med Biogr. 11: 232–240 (2003)