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Neurology > Guillain Barre Syndrome > Flashcards

Guillain Barre Syndrome Flashcards

1
Q

What is spinal shock?

A

In an UMN pathology when at first patient can get initial normal tone and absent reflexes. Later, classic UMN lesions would emerge.

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2
Q

What investigations would be done for presentation of four limb weakness?

A
  • FBC, U+Es, LFTs, Ca, phosphate, Mg
  • CRP + ESR
  • CXR (for SOB)
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3
Q

What are the characteristic features of GBS?

A
  • Progressive symmetrical weakness of all 4 limbs
  • Weakness is classically ascending i.e. legs are affected first
  • Reflexes are reduced/absent
  • Sensory symptoms tend to be mild e.g. distal paraesthesia with sensory signs
  • Back/leg pain in initial stages of illness
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4
Q

What are other features of GBS?

A
  • May be a history of gastroenteritis - campylobacter
  • Respiratory muscle weakness
  • Cranial nerve involvement: diplopia, bilateral facial nerve palsy, oropharyngeal weakness
  • Autonomic involvement: urinary retention, diarrhoea
  • Less common: papilloedema (thought to secondary to reduced CSF resorption
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5
Q

What are the investigations for GBS?

A
  • Lumbar puncture: rise in protein with normal WBC count (albuminocytologic dissociation), <10 cells and normal glucose
  • Nerve conduction studies: decreased motor nerve conduction velocity (due to demyelination), prolonged distal motor latency, increased F wave latency
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6
Q

What is Guillain-Barre Syndrome?

A
  • GBS is a poly-radiculo-neuropathy
  • Predominantly motor disorder, some sensory symptoms
  • No sphincter disturbance or encephalopathy
  • No sex difference
  • Affects all ages but is slightly more frequent in older age range
  • Most common cause of acute neuromuscular weakness in developed world
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7
Q

What are the types of GBS?

A
  • Acute inflammatory demyelination polyradiculoneuropathy (AIDP)
  • Acute motor axonal neuropathy (AMAN)
  • Acute motor and sensory axonal neuropathy (AMSAN)
  • Miller-Fisher syndrome
  • Pure sensory neuropathy
  • Acute pandysautonomia
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8
Q

What are time ranges for the duration of these disorders?

A
  • Acute - peak disability by 4wks
  • Subacute - 4-8wks
  • Chronic - >8wks
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9
Q

Describe AIDP

A
  • 2/3 have identifiable trigger
  • Begins with paraethesias and pain followed by muscle weakness in legs (10% begins in arms and rarely in face)
  • Complete ophthalmoplegia in 3-5%, partial 15%
  • Autonomic manifestations: labile BP, arrhythmia, constipation, abdominal distension
  • Progresses days to 4 weeks
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10
Q

What are the differential diagnoses of GBS?

A
  • Acute myelopathies
  • Botulism
  • Diphtheria
  • Lyme disease and tick borne paralyses
  • Porphyria
  • Vasculitis neuropathy
  • Poliomyelitis
  • CMV polyradiculitis
  • Critical illness neuropathy
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11
Q

What is the therapy for GBS?

A
  • Thromboprophylaxis - TEDS and sc LMWH
  • Respiratory obs - FVC, if ABGs/RR/SaO2 abnormal then often patient will be in peri-arrest. Don’t be afraid to intubate and refer to ITU at signs of respiratory problems.
  • IPPV if FVC <15ml/kg
  • IV immunoglobulin 0.4g/kg/day for 5 days (evidence in non-ambulant patients)
  • DO NOT use corticosteroids
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12
Q

What infections can trigger GBS?

A 
Viral:
- EBV
- HIV
- Influenza
- Hep A+C
Bacterial: 
- Campylobacter jejuni
- Mycoplasma pneumoniae
- E. coli
- Haemophilius influenzae
Parasites:
- Malaria
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13
Q

What systemic illnesses can trigger GBS?

A
  • Hodgkin’s disease
  • Hyperthyroidism
  • Sarcoidosis
  • Renal disease
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14
Q

What other medical conditions can trigger GBS?

A
  • Pregnancy
  • Surgery
  • Bone marrow transplant
  • Immunisation
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15
Q

How does campylobacter jejuni cause GBS?

A

This is a common cause, different strains can have different effects. Shared epitopes lipo-oligosaccharide and human gangliosides (antibody attacks its own tissues) (molecular mimicry).

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16
Q

What are the normal ranges for measurements in lumbar puncture?

A
  • Opening pressure (patient needs to be lying down) <20cm
  • WCC <5 WBC
  • RCC none
  • Protein <0.45g/l
  • Glucose approx 2/3 of plasma (check blood glucose at same time) - 50-66
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17
Q

What are extra tests that can be performed on the CSF?

A
  • Microbiological stains
  • Culture and sensitivity
  • Viral/bacterial PCR
  • Oligoclonal bands
  • Cytology (requires at least 10ml of CSF, so is difficult to perform)
  • Spectrophotometry/xanthocromia - spectrophotometry looks for oxyhaemoglobin and bilirubin peaks
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18
Q

What are the bacterial results of an LP?

A
  • Opening pressure (cm) - high
  • Cells - 100-50,000 (neutrophils)
  • Protein (g/l) - >1.0
  • Glucose (% of plasma) - <40
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19
Q

What are the viral results of an LP?

A
  • Opening pressure (cm) - normal
  • Cells - 5-1000 (lymphocytes)
  • Protein (g/l) - 0.5-1.0
  • Glucose (% of plasma) - 50-66
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20
Q

What are the tuberculosis results of an LP?

A
  • Opening pressure (cm) - high/very high
  • Cells - 5-500 (lymph)
  • Protein (g/l) - 1.0-5.0
  • Glucose (% of plasma) - <33
21
Q

What are the fungal results of an LP?

A
  • Opening pressure (cm) - very high
  • Cells - 0-1000 (lymph)
  • Protein (g/l) - 0.5-2.0
  • Glucose (% of plasma) - 30-50
22
Q

What are the characteristic features of TB in CSF?

A
  • Very low glucose, less than 1/3 of plasma
  • Very high protein (sometimes >5 g/l)
  • Very high opening pressure
  • Lymphocytosis
23
Q

What does MS look like in CSF?

A
  • Often normal CSF, except oligoclonal bands +ve

- Oligoclonal bands would not be seen in normal blood, hence limited to CNS

24
Q

What would cancer look like in CSF?

A
  • High WBC and protein
  • Very low glucose
  • Abnormal cytology
25
Q

What would SAH look like in CSF?

A
  • High RBC

- Xanthacromia (sensitive after 12hrs) - raised bilirubin and oxyhaemoglobin

26
Q

What results from an LP can you get in herpes simplex encephalitis?

A

Commonest viral encephalitis

  • Haemorrhage CSF (raised RBC count)
  • Viral infection: lymphocytes, modest elevation in protein, normal glucose
27
Q

What is transverse myelitits?

A
  • Acute inflammation of grey and white matter in >/= 1 adjacent spinal cord segments, usually thoracic
  • Causes: MS, neuromyelitis optica, infections, autoimmune or post infectious inflammation, vasculitis and certain drugs
  • If the patient presents with signs of myelopathy (spinal cord syndrome) + CSF has unmatched oligoclonal bands, consider transverse myelitis, need more clinical info to rule out MS
28
Q

What is acute cervical cord syndrome?

A
  • Patients presenting with this would be expected to have a mixture of 4 limb motor and sensory signs, some have pain
  • Many patients will have sphincteric symptoms - bladder urgency and frequency
  • Examination may show increased tone and brisk reflexes in all 4 limbs. However, in very acute cord syndromes tone may be flaccid and reflexes absent (spinal shock).
  • Some patients will have a sensory level on the chest determined by pin prick sensory examination
  • In patients with posterior cord involvement there may be no motor symptoms or signs - these patients may be very unsteady due to sensory ataxia
29
Q

What are the features of cauda equina syndrome?

A
  • Patients presenting with this will have lower limb signs and symptoms but normal upper limbs. Most will have motor and sensory problems.
  • Pain may be present, especially if syndrome is due to compressive pathology
  • Examination will reveal LMN signs
30
Q

What are the symptoms of cauda equina syndrome?

A
  • Loss of sensation around buttocks, anus, genital (saddle anaesthesia)
  • Shooting pain down back/side of legs
  • Bladder + bowel incontinence
  • Lack of sensation +/or weakness in legs
31
Q

What are the features of Myasthenia Gravis?

A
  • Autoimmune condition - patients muscles become weak after use, no sensory problems (functional fatigue) - get patient to move limb and test power before and after
  • The weakness can affect any muscle, typically affected areas include eyes (ptosis, diplopia), mouth (dysarthria + dysphagia) + proximal limbs, proximal myopathy with symptoms worse at the end of the day (face, mask, limb girdle)
  • Respiratory muscles, check for SOB, especially when lying down (weak diaphragm)
  • Weakness is fatigable
  • Thymoma
  • Other autoimmune disorders: pernicious anaemia, thyroid disorders, RA, SLE
32
Q

What are the investigations for myasthenia gravis?

A
  1. ACh receptor antibodies
  2. If negative then neurophysiology with repetitive stimulation +/- single fibre studies (electron myography to see fatigue ability of nerves)
  3. CT thorax do exclude thymoma (common in young people) and MRI brain to exclude pathology - not diagnostic
  4. Put ice on ptosis: diagnostic of MG if it resolves
33
Q

What is the management of myasthenia gravis?

A
  • Long acting AChE inhibitors e.g. pyridostigmine
  • Immunosuppression: prednisolone initially
  • 3rd line: cyclophosphamide, monocloncal antibodies e.g. rituximab
  • Thymectomy
  • Management of myasthenic crisis: plasmapheresis (plasma removed from body, either replaced by saline/albumin, or treated and returned to body) + IV immunoglobulins
34
Q

What is acute myosotis?

A
  • Symmetrical, proximal muscle weakness + myalgia
  • Progresses over weeks to months (insidious onset)
  • Usually neck, shoulders and pelvis affected first
  • Often mild - can find it difficult to walk upstairs, standing up
  • Rare: can get dysphagia/dysarthria
  • Associated with ILD, Raynaud’s phenomenon, polyarthritis, SLE
  • On examination, reflexes and sensation should be normal
35
Q

What is dermatomyositis?

A
  • Polymyositis only affects muscle, but dermatomyositis involves skin as well
  • Signs: heliotrope rash (butterfly rash on face, similar to malar rash in SLE)
  • Gottron’s papules- erythematous scaly lesions specifically on MCPs, PIPs, DIPs (this confirms diagnosis for dermatomyositis)
  • Gottron’s sign - scaly lesions found beyond the hands, like elbows, neck etc
  • Shawl sign - hyperpigmented skin (rash) on shoulders, neck and upper back
  • V sign - rash on neck and upper chest
  • Holster sign - rash on lateral thigh
  • Periungual erythema - redness around fingernails
  • Calcionosis cutis - calcium deposits under skin (usually in kids, very painful)
36
Q

What are the investigations for dermatomyositis?

A
  • Creatine kinase
  • ALT + AST - leaks out of muscles
  • ANA
  • Autoantibodies: Anti-Jo, Anti-Mi, Anti-SRP
  • EMG
  • Muscle biopsy - muscle inflammation and fibrosis
37
Q

What are the treatments for dermatomyositis?

A
  • Corticosteroids
  • Immunosuppression e.g. methotrexate
  • Hydroxychloroquine - dermatomyositis rash
  • Physical and occupational therapy
  • Assess for possible malignancies
38
Q

What do the results of nerve conduction testing mean?

A
  • As long as the nerve speed is >49m/s for a motor nerve, the result is normal
  • If it’s <49m/s there is a problem with the myelin sheath surrounding the nerve - can indicate demyelinating neuropathy
  • The waveform/amplitude of the graph (when conducting study) displays the strength of the muscle twitch - if it’s not the right shape it can indicate nerve axon damage (being cold can slow nerve impulses)
39
Q

What is acute cervical cord syndrome/central cord syndrome?

A
  • Weakness in upper extremities (arms) + less severe weakness of lower extremities (legs)
  • Difficulty getting dressed
  • Often affects 50+ who have sustained neck (cervical) hyperextension injury
40
Q

What are the causes of cervical cord syndromes?

A
  • Inflammatory - MS, post infective, NMO/Devic’s, CTD related
  • Compressive - discs, tumours
  • Infective - viral (VZV, HIV)
  • Metabolic (B12, copper deficiency)
41
Q

What is a supinator catch?

A

Hyperreflexia and contraction of muscle groups not expected in the usual reflex - extra movements (problem with spinal cord across myotomes).

42
Q

How would bladder/bowel issues present in U/LMN lesions?

A

LMN lesion: won’t be able to feel they have a full bladder and need to go to toilet
UMN lesion: urge incontinence

43
Q

What are the causes of ptosis?

A
  • Myasthenia Gravis - weakness starts in face and descends, bilateral ptosis, ocularbulbar lesion
  • Horner’s - unilateral, lower medullary lesion
  • 3rd nerve palsy - unilateral, midbrain lesion
44
Q

What is myelopathy?

A

Anything affecting spinal cord (spinal lesion)

45
Q

What is myeloradiculopathy?

A

Nerve root/radicals affected - shooting pain

46
Q

Describe the symptoms of damage to the anterior spinal artery

A
  • Affects anterior 2/3s of spinal cord
  • Dorsal column spared
  • Ascending spinothalamic and descending corticospinal tract affected below level of lesion - weakness in all limbs
  • Reflexes absent in beginning - flaccid, not spastic
  • Sensory change and acute onset
47
Q

What is syringomyelia/bulbia?

A

Fluid filled cyst within the spinal cord (bulbia extends to Brainstem - medulla)

  • Compression of spinal cord - pain, weakness, stiffness
  • Swallowing difficulties
  • Lose pain and temperature in hands bilaterally
  • In medulla can affect cranial nerves causing facial palsies
48
Q

What is the significance of B12 deficiency with spinal cord symptoms?

A

Damages dorsal columns and corticospinal tracts - combined degeneration. Nitrous oxide precipitates this, causes a functional deficiency in B12 so need to ask in history.
Tx: replace B12

49
Q

What are the causes of spinal cord conditions? VIN MDT

A 
Vascular/vasculitic
Infected/inflammatory
Nutritional/neurodegenerative
Metabolic/mitochondrial
Developmental/degenerative
Toxic/trauma

Neurology (5 decks)

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