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Neuro and geriatrics > Muscle weakness > Flashcards

Muscle weakness Flashcards

1
Q

What are the 2 types of descending tracts?

A

Pyramidal tracts

Extrapyramidal tracts

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2
Q

Where do the pyramidal tracts originate?

A

Cerebral cortex

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3
Q

What is the function of the pyramidal tracts?

A

Voluntary control of musculature of body and face

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4
Q

Where do the pyramidal tracts pass through?

A

Medulla oblongata

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5
Q

Name the 3 pyramidal tracts

A

Corticospinal tracts - lateral and anterior

Cortiobullar

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6
Q

Where do the extrapyramidal tracts originate from?

A

Brainstem

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7
Q

What is the function of the extrapyramidal tracts?

A

Involuntary and automatic control of all musculature such as muscle tone, balance, posture and locomotion

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8
Q

Name the 4 extrapyramidal tracts

A

Vestibulospinal and reticulospinal (these don’t decussate)

Rubrospinal and tectospinal (decessate)

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9
Q

Where does the corticospinal tract divide into the lateral and anterior?

A

Caudal part of medulla

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10
Q

What is the route of the lateral corticospinal tract?

A

Decussates at medulla and terminates in ventral horn at segmental levels

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11
Q

What is the route of the anterior corticospinal tract?

A

Remains ipsilateral decussates in cervical and upper thoracic segmental levels

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12
Q

Which cranial nerve is NOT part of the PNS?

A

CN II

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13
Q

Where does the spinal cord end?

A

L1

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14
Q

What information about muscle weakness is important to get in a history?

A

Onset - instant/gradual
Distribution - proximal/distal, symmetrical/asymmetrical, mono (local process)/poly (diffuse), cranial involvement (bulbar/ophthalmoplegia/facial)
Variability - fatigueability/relapse-remission
Additional features - sensory symptoms (paraesthesia/loss of sensation)
Contact - recent illness, PMH, FH, drugs, alcohol

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15
Q

What the the UMN signs?

A 
Bulk - normal
Tone - increased
Strength - decreased
No fasciculations
Increased reflexes
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16
Q

What are the LMN signs?

A 
Reduced (wasting) bulk
Normal/decreased tone
Decreased strength
Fasciculations
Decreased/absent reflexes
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17
Q

How is muscle power graded?

A

MRC grading

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18
Q

What does 0 mean on MRC grading?

A

Complete paralysis

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19
Q

What does 1 mean on MRC grading?

A

Flicker of contraction possible

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20
Q

What does 2 on MRC grading mean?

A

Movement possible if gravity eliminated - hold elbow up and see if can extend

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21
Q

What does 3 on MRC grading mean?

A

Movement against gravity but not resistance

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22
Q

What does 4 on MRC grading mean?

A

Movement possible against some resistance

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23
Q

What does 5 on MRC grading mean?

A

Power normal (not normally possible to overcome a normal adult’s power)

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24
Q

Name 2 causes of weakness

A

Neuropathies

Myopathies

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25
Q

Name 3 causes of neuropathies

A

Peripheral neuropathy
GBS
MG
MND

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26
Q

How are neuropathies classified?

A 
Polyneuropathy (peripheral neuropathy)
Mononeuropathy multiplex (mononeuritis multiplex) - at least 2 nerves
Mononeuropathy - one single nerve
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27
Q

What is a peripheral neuropathy?

A

Disease affecting peripheral nerves

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28
Q

What might be the S&S of a peripheral neuropathy?

A

Chronic and slowly progressive
Starting in legs and longer nerves
Sensory/motor/both

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29
Q

What conditions cause predominantly motor loss in peripheral neuropathy?

A 
GBS
CIDP
HSMN
Diphtheria
Porphyria
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30
Q

What condition cause predominantly sensory loss in peripheral neuropathy?

A 
Deficiency states eg B12/folate
Diabetes
Alcohol/toxins/drugs
Metabolic abnormalities eg uraemia
Leprosy
Amyloidosis
31
Q

What is mononeuritis multiplex?

A

Painful, asymmetrical sensory and motor neuropathy
Subacute presentation
Immune/inflammation mediated

32
Q

What causes mononeuritis multiplex?

A

Vasculitis eg churg strauss

Connective tissue disorder eg sarcoid

33
Q

What is a mononeuropathy?

A

Individual nerve deficits in isolation

Upper limb nerves mostly affected at compression points

34
Q

What is the most common mononeuropathy?

A

Median nerve entrapment at wrist

Carpel tunnel

35
Q

What other nerves can get trapped in the upper limb and what does it look like?

A

Ulnar nerve at elbow (claw hand)

Radial nerve at axilla (wrist drop)

36
Q

Which nerve entrapment in the leg is most common?

A

Common peroneal nerve (foot drop)

37
Q

What investigations might you do in a neuropathy investigation?

A 
Neuropathy screen (looks at screen)
Vasculitis screen
EMG/NCS
CSF study
Imaging/nerve biopsy
38
Q

What happens in a neuropathy screen?

A

Bloods

  • FBC, ESR
  • U&E, glucose, TFT, CRP, serum electrophoresis
  • B12/folate
  • Anti-gliadin
  • TPHA, HIV
39
Q

What happens in a vasculitis screen?

A

FBC, ESR
U&E, Cr, CRP
ANA, ANCA, anti-dsDNA, RhF, complement, cryoglobulins

40
Q

What is the treatment of neuropathy?

A

20% idiopathic with no treatment
Neuropathic analgesic - gabapentin, pregabalin, amitryptiline
Treat/remove underlying cause eg DM/B12 deficiency
Inflammatory neuropathy - prednisolone with steroid sparing agents
Vasculitis - prednisolone with immunosuppressant

41
Q

What is GBS?

A

Autoimmune response causing demyelination

42
Q

When might GBS occur?

A

Post infections - resp/GI eg campylobacter

43
Q

How does GBS present?

A

Subacute (< 6 weeks) ascending paralysis/numbness/areflexia

Always ask about breathing and swallowing!!

44
Q

What will NCS studies show in GBS?

A

Demyelination

45
Q

What will LP show in GBS?

A

Raised CSF protein

46
Q

How do you treat GBS?

A

IV Ig or plasmapheresis
Support
Monitor FVC
ITU review

47
Q

How long can recovery from GBS take?

A

Weeks - years

48
Q

What is myasthenia gravis?

A

Autoimmune disorder - antibodies against nicotinic acetylcholine receptors in the NMJ characterised by weakness and fatigueability of proximal limb, bulbar and ocular muscles
Potentially fatal but treatable condition

49
Q

What is also common in MG?

A

Thymus dysfunction - hyperplasia/thymoma

50
Q

What are the S&S of MG?

A 
Generalised - fatigueable weakness - proximal limbs, neck and face (head drop, ptosis), extraocular (complex diplopia), bulbar (speech/swallow) particularly elderly
Ocular
At risk of other autoimmune diseases
Facial expression - myasthenic snarl
Ptosis, diplopia
Tendon reflexes normal  but fatigueable
Symptoms worse towards end of day
Respiratory difficulties
May fluctuate in severity over time
51
Q

What investigations should you do for MG?

A

Tensilon test (allow accumulation of Ach in NMJ) - give IV edrophonium (short-acting anti-cholinesterase) - muscle power increases within seconds
AchR antibodies (raised in 90%) and MuSK antibodies (anti-muscle specific tyrosine kinase)
EMG - looks at NMJ and NCS
CT thorax/MRI - hyperplasia/atrophy/tumour

52
Q

How do you treat MG?

A

Acetylcholinesterase inhibitors - symptomatic treatment
Immunosuppressants - steroids (start slowly), azathioprine, methotrexate, mycophenolate
Thymectomy if onset < 50 and disease poorly controlled with anti-cholinesterases

53
Q

What is a myasthenic crisis?

A

Severe weakness including respiratory muscles
High risk of death
Always ask about breathing and swallowing!!

54
Q

What can cause a myasthenic crisis?

A

Infection
Natural disease cycle
Underdosing and overdosing of medication

55
Q

How do you treat a myasthenic crisis?

A

Take change in myasthenic condition seriously
Urgent review by neurologists
Think about breathing and monitor FVC
Anaesthetist review
Plasmapheresis and IV Ig to identify and treat trigger of relapse

56
Q

What is MND?

A

Degeneration of motor neurons in the motor cortex and anterior horns of spinal cord
Mainly clinical diagnosis

57
Q

How does MND present?

A

UMN and LMN signs
No sensory, visual or bladder/bowel involvement
Asymmetrical weakness
Bulbar/limb onset

58
Q

What investigations should you do for MND?

A

LP
NCS/EMG
MRI

59
Q

What is the most common type of MND?

A

ALS

60
Q

What is the survival rate of MND?

A

2-5 years

61
Q

What are the most common muscle disorders?

A

Steroid myopathy
Statin myopathy
Metabolic and endocrine myopathies
Myotonic dystrophy

62
Q

What are the uncommon muscle disorders?

A

Muscular dystrophies eg Duchenne, Becker, facioscapulohumeral musclar dystrophy
Inflammatory muscle disease - polymyositis/dermatomyositis
Mitochondrial disorders

63
Q

What are the symptoms of muscle disorders?

A 
Stairs, chairs, and hair
Wasting common
Facial weakness
Neck weakness
Contractures
Scoliosis
Eye movement disorders rare
64
Q

What investigations should you do in muscle disorders?

A 
CK
EMG
ESR/CRP
Genetics DMD
Biopsy
65
Q

How do you treat muscle disorders?

A

Remove causal agent if is one
Supportive - physio, OT, back, renal, diet
Immunosuppress if inflammatory

66
Q

How common is MG?

A

More common in women 2:1
Peak age of incidence 30 with another smaller peak of incidence in men over 60
Prevalence 4 in 100,000

67
Q

What can cause MG?

A

Under 50 and in women - other autoimmune diseases eg pernicious anaemia, SLE, rheumatoid arthritis, thymic hyperplasia
Over 50 and in men - thymic atrophy or thymic tumour, rheumatoid arthritis, SLE
Transient MG - D-penicillamine treatment for Wilson’s

68
Q

What is the pathology of MG?

A

Autoimmune disease mediated by antibodies to nicotinic acetylcholine receptor - anti-AChR antibodies, interfering with NMJ via depletion of working post-synaptic receptor sites
Achieved by immune complex deposition of anti-AChR IgG and complement at post-synaptic membranes causing interference with and destruction of receptors
Both B and T cells implicated
Blocks excitatory effect of Ach on the nicotinic receptors due to less receptors resulting in muscle weakness

69
Q

How can you demonstrate fatigueability in MG?

A

Ask patient to count to 50 - as reach higher numbers, voice becomes less audible
Hold finger up high and ask patient to look at it without lifting head - after a few seconds will be unable to keep eyes raised

70
Q

What might worsen MG symptoms?

A

Pregnancy, hypokalaemia, infection, emotion, exercise, drugs

71
Q

What drugs might worsen MG symptoms?

A

Opiates, beta-blockers, gentamicin, tetracycline

72
Q

What could be differentials for MG?

A

MS
Hyperthyroidism
Acute GBS
Lambert-Eaton myasthenic syndrome

73
Q

What is Lambert-Eaton myasthenic syndrome?

A

Paraneoplastic condition most often seen with small cell lung cancer due to defective Ach release at NMJ
Causes defective Ach release at NMJ resulting in proximal limb weakness with some absent reflexes
Weakness tends to improve after exercise - unlike MG

74
Q

What are the S/E of anti-cholinesterases?

A

Increased salivation, lacrimation, sweating
Vomiting
Miosis (excessive pupillary constriction)
Diarrhoea

Neuro and geriatrics (21 decks)

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