Weakness Flashcards

1
Q

How to describe clinical weakness:

A

First decide: Neuromuscular vs Non-NM cause

Global/ focal
Bilat/ unilat
Proximal/ distal

Patterns of:
UMN
LMN
NMJ
Myopathy

Strength (Gr 0-5)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Scale of motor strength:

A

5- Against full resistance
4- Against mild resistance
3- Against gravity
2- Gravity eliminated
1- Flicker
0- Nil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Features that differentiate:
- UMN
- LMN
- NMJ
- Myopathy

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the ‘pyramidal’ pattern of weakness?

A

Suggests UMN.

Weakness of:
- Upper limb extensors
- Lower limb flexors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

DDx of weakness:

A

NON-NEUROMUSC- subjective, global
- Anaemia
- Sepsis
- CCF
- SLE, fibromyalgia, chronic fatigue
- Hypothyroidism
- Electrolytes (Na, Ca, K)

NEUROMUSCULAR WEAKNESS- quantitative loss of strength
Brain
- Stroke
- SOL
- Multiple sclerosis

Cord
- Compression
- Infarct
- Stenosis
- Abscess

NMJ
- Myaesthenia gravis
- Lambert-Eaton (paraneoplastic)

Myopathy
- Statins
- Steroids
- Addison’s
- Cushing’s
- Thyrotoxicosis
- Myositis
- Muscular dystrophy

Toxic/toxin
Organophosphates
Botulism
Tetanus
Ciguatera
Paralysis tick
Blue-ringed octopus
Snake-bite (Taipan)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Bell’s Palsy: assessment and DDX

A

Facial nerve (CN VII) palsy
–> Facial weakness to whole half of face (incl forehead and eye).
–> Salivation
–> Tears
–> Taste on anterior 2/3 tongue

‘Bell’s is idiopathic

MUST LOOK FOR EAR VESICLES (Ramsay-Hunt) Prognosis much worse.
- Parotid mass
- Cholesteatoma
- Acoustic neuroma
- Brainstem event

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Bell’s Palsy Mx:

A

PREDNISOLONE 1mg/kg for 7 days
(2mg/kg paeds)
+
- ACICLOVIR 10mg/kg PO 5x daily (if within 72 hours)**
(Cover for pre-rash Ramsay Hunt)

Eye drops/ ointments
Tape eye nocte

PROGNOSIS
- Most better by 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Clinical features of Guillian-Barre:

A

Acute autoimmune neuropathy of nerve roots and peripheral nerves (LMN)
1- Demyeliation
or
2- Axonal

Follows < 3 weeks after a Resp or GI illness
- Campylobacter most common
- Mycoplasma, Hib, CMV, EBV.

Onset over days to weeks

Causes Symmetrical ASCENDING paralysis
- Flaccid, tendon reflexes absent
- ALL: limbs, trunk, resp
- MOST: cranial nerves, sensory
- SOME: eyes
- A FEW: autonomic dysregulation
Worst at 2-4 weeks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which GBS type is most common with Campylobacter?

A

Direct AXONAL neuropathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diagnosis of Guillian-Barre:

A

Mostly clinical diagnosis
- Preceding resp/GI illness
- Symmetrical, ascending flaccid paralysis

Adjunctive:
- MRI C spine
- Lumbar puncture
–> Protein rise without WCC
- Resp and stool screen
- Lung functions tests (serial, to guide elective intubation)
- Evoked potentials (not ED)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Management of Guillian-Barre:

A

Focus on airway and ventilatory support

Manage secretions
Check lung function 2-hourly (VC, peak flow)
Intubate + ventilate for deteriorating:
- FVC (<15ml/kg)
- FEV1/FVC (<50% predicted)
- Peak flow (<250ml/min)
- NO SUX
- Will need mandatory mode (weak)
NIV NOT RECOMMENDED.

IVIG (2g/kg over 5days)
or
Plasma exchange

FASTHUGS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Mortality in Guillian-Barre:

A

Majority recover completely (but slowly)

20% will have persisting neuro deficit

Death usually resp failure or autonomic dysFx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the Miller-Fischer variant in GBS?

A

Cranial nerves FIRST.

Oculomotor palsy –> limb weakness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Tetanus:

A

Opisthotonos and trismus
Resp failure +/- autonomic dysFx

Clostridium tetani (soil)

More common where no imm, poorly tended wounds (eg. homeless)

Supportive
Tetanus immunoglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Periodic paralysis

A

Rare channelopathy causing periodic attacks of weakness that last minutes, up to 3 days before resolving suddenly.

Vary in severity and duration

Onset usually in childhood

Triggers:
- High carbs
- After strenuous exercise
- Stress/ excitement
- Sudden temp changes

Types:
- Hypokalaemic periodic paralysis- most common
- Hyperkalaemic
- Thyrotoxic

Mx:
- Supportive
- UEC/CMP- K+ NOT ALWAYS LOW
- Thyroid function
- Replenish K+
- Prophylaxis (eg. acetazolamide, diet)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Multiple Sclerosis: clinical features

A

Immune-mediated chronic demyelinating condition affecting brain and cord white matter (UMN)

Women
Tasmania
Age 15-45 at onset

Heat/fever can trigger relapse.

Relapses = almost anything:
- Optic neuritis + other visual COMMON
- UMN pattern weakness (spastic, prox)
- Painful shocks in legs

17
Q

Multiple Sclerosis: Diagnosis

A

Lumbar puncture:
- High protein
- Pleocytosis with predominant lymphocytosis (mild)
- OLIGOCLONAL BANDS

MRIB
- Multiple white matter plaques on T2
–> Subcortical OR periventricular
Not visible during remissions

18
Q

Multiple Sclerosis: Treatment

A

1g IV Methylprednisolone
or
Plamapharesis

19
Q

Myaesthenia Gravis: Clinical features

A

Autoimmune attack on post-synaptic AcH receptors (LMN)

Idiopathic.

Exacerbations triggered by illness or stresses

Causes weakness, that is fatiguable and relieved by rest
- Usuallyfacial/ bulbar
–> Ptosis
–> Dysphonia
–> Dysarthria

‘Myaesthenic crisis’ = generalised weakness and resp compromise (20%)

20
Q

Myaesthenia Gravis: diagnosis

A

Clinical features

Anti-AcH antibodies in blood

21
Q

Myaesthethenia Gravis: management

A

Supportive
–> Unlike GBS, NIV is recommended option

IVIG
Plasmaphoresis
Steroids can make worse

Long term ‘stigmine

22
Q

Eaton-Lambert syndrome:

A

Like the ‘opposite’ of myaesthenia

Autoimmune paraneoplastic syndrome, typically SCLC

Attack on PREsynaptic release of AcH.
IMPROVES with exercise

Only treatment, is to treat the cancer.

23
Q

Motor neurone disease (ALS- amyotrophic lateral sclerosis)

A

Mixed UMN and LMN destruction. Rapidly progressive, death within 2-4 years.

Bulbar and respiratory weakness are most prominent:
–> Choke, aspiration
–> Resp failure

Mixed nature: often spastic weakness but with fasciculations

Most ED presentations will be resp (aspiration or failure). Management is supportive:
- Try to avoid NIV (aspiration, more WOB)- HFNP better
- NO opiates - resp drive depression

24
Q

What is the ‘icepack test’

A

Patient with ptosis

Apply icepack to face for 2 mins

If immediately resolves- likely myaesthenia

25
Q

Botulism:

A

Clostridium botulinum

In adults, toxins in food poisoning (partic home-canned). In infants, spores in honey.

Inhibits Ach at presynaptic

Starts with bulbar –> DESCENDING flaccid paralysis

Botulism antitoxin