25. Weakness Flashcards

1
Q

differential for weakness

A

Brain
- MS
- Stroke (and think about stroke mimics hypoglycaemia, todd’s paresis, migraine, bell’s palsy)
- Space occupying lesion
- Psychogenic

Spinal Cord
- MS
- Motor neuron disease
- Myelopathy
- Any spinal cord disorder affecting the corticospinal tract eg subacute combined degeneration,

Nerve roots
- Radiculopathy

Peripheral nerves
- Motor neuron disease causing LMN signs
- peripheral neuropathy - motor loss

Neuromuscular junction
- Myasthenia gravis and lambert eaton

Muscle
- Muscular dystrophy
- Muscular breakdown eg rhabdomyolysis
Muscle inflammation and damage eg rhabdomyolysis, polymyositis, dermatomyositis, statin-induced, corticosteroid induced, cushings, addisons

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2
Q

History taking weakness

A

PC: weakness = onset? where in the body, has the pattern changed? worse at any point in the day? how does it affect ADLs?, improved by rest or movement?

screening for weakness elsewhere: eyelid weakness? double vision? lazy eye? change in vision (eg homonymous hemianopia), facial expression weakness? difficulty getting up from a chair? clumsy? difficulty swallowing?speaking?

associated symptoms: headache, n&v, LOC, changes to voice? dizziness? vertogo? palpitations

MHx: AF, migraines,
DHx: anticoagulants, statins, COCP,

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3
Q

Examination weakness

A

UL neuro, LL neuro
- any UMN signs?
- pattern of weakness?

Cranial nerve exam
- eye movements?
- visual field defect?
- forehead sparing?
- swallowing issue?

GCS

cerebellar exam

ABCDE
check glucose!! can cause stroke mimic!

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4
Q

UMN signs

A

Minimal muscle atrophy
Weakness
Hyperreflexia of deep tendon reflexes- as no UMN regulating that reflex
Absent superficial reflex - babinski positive
Hypertonia + or - clonus
Pronator drift

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5
Q

causes of LMN lesions

A

ALS (may also have UMN)

Peripheral neuropathy motor loss (guillain barre, charcot-marie tooth)

Spinal cord disorders (should also have UMN) that involve:
Injury to axons leaving spinal cord
Injury to anterior horn/grey matter of spinal cord

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6
Q

causes of UMN lesions

A

Stroke
Infection
Tumour
Damage to white matter/corticospinal tract eg myelopathy, MS
ALS
Injury to brain stem

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7
Q

LMN signs

A

Muscle atrophy
Flaccid paralysis
No plantar response
Absent tendon reflexes
Fasciculations (single muscle fibres of uninjured LMN stimulated)

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8
Q

test for conversion disorder weakness

A

hoovers sign

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9
Q

causes of peripheral muscle weakness? signs?

A

guillian barre
Charcot-marie tooth
lead poisoning

Ascending weakness
“Tripping over feet”
Foot drop
Hyporeflexia

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10
Q

causes of proximal muscle weakness

A

Corticosteroid-induced proximal myopathy
Statin-induced myopathy
Cushings
Rhabdomyolysis
Polymyositis
Dermatomyositis
Addisons
Muscular dystrophy

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11
Q

Presentation polymyositis and dermatomyositis

A

Symmetrical, proximal muscle weakness
Raynaud’s

As the disease progresses, other muscles may also become involved, resulting in the following:
Pharyngeal or oesophageal muscles leading to dysphonia and dysphagia.
Respiratory muscles can lead to poor ventilation with type 2 respiratory failure.

Dermatomyositis causes the above plus skin changes eg
Heliotrope rash -which is a lilac discolouration of the eyelid skin in addition to periorbital oedema

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12
Q

first line invetsigation ?inflammatory myopathy

A

creatinine kinase

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13
Q

invetsigations ?polymypositis/dermatomyositis

A

creatinine kinase

nerve conduction studies = Electromyography (EMG)

muscle biopsy for definitive

may want to look for underlying malignancy

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14
Q

what enzymes are elevated in demratomyositis and polymyositis

A

DM and PM turn your muscles into CLAAA (clay):

Creatine kinase
Lactate dehydrogenase
Aldolase
ALT
AST

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15
Q

management polymyositis/dermatmyositis

A

Corticosteroids

are the mainstay of treatment. They are started at high doses initially, creatanine kinase is then monitored to guide the rate of tapering the dose.
Many patients need an additional immunosuppressant such as methotrexate or azathioprine as a steroid-sparing agent.
Hydroxychloroquine occasionally helps with skin disease in dermatomyositis.
As well as pharmacological therapy, physiotherapy is essential to rehabilitate patients.

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16
Q

define stroke

A

‘rapidly developing clinical signs of focal (at times global) disturbance of cerebral function, lasting more than 24 hours or leading to death with no apparent cause other than that of vascular origin

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17
Q

define TIA

A

a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction

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18
Q

Approach to acute assessment of ?stroke

A

ABCDE
A
B - is there increased RR? (get blood gas as may be hyperventilating causing resp alk) maintain O2 sats
C - BP- monitor this- in haemorrhagic this is sometimes lowered. Get ECG (may have AF)
D - Don’t forget glucose!!!, reduced GCS may indicate haemorrhagic
E
Focused UL, LL, cranial nerve examination and cerebellar exam

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19
Q

should BP be managed during stroke

A

ischaemic - usually no, except if:
hypertensive encephalopathy
Hypertensive nephropathy
Hypertensive cardiac failure/myocardial infarction
Aortic dissection
Pre-eclampsia/eclampsia

haemorrhagic - sometimes yes, consult local guidelines

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20
Q

what is the ROSIER score

A

score used in ?stroke to help ddx between stroke and stroke mimics

a score > 0 means stroke likley

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21
Q

what scoring sytem will you use when assessing ?stroke

A

ROSIER

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22
Q

what is part of rosier score

A

LOC -1
seizure -1

asymmetric facial weakness +1
asymmetric arm weakness +1
asymmetric leg weakness +1
speech disturbance +1
visual field defect +1

A stroke is likely if > 0

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23
Q

first line for investigation ?stroke

A
  1. non contrast CT
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24
Q

what can a non-contrast CT show you in stroke

A

ischaemic
- hyperdense artery (often visible immediately)
- low density in grey/white matter (takes time to develop)

haemorrhagic
- hyperdense material (blood) surrounded by low density (oedema)

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25
if a non-contrast CT shows ishcameic stroke/rules out haemorrhage, what other scans might you get?
CT angiography particularly if thrombectomy is being considered MR angiography CT perfusion scan or diffusion weighted MRI if looking for salvagable brain tissue
26
risk factors for ischaemic stroke
OCP is a risk factor Migraine is a risk factor AF is a risk factor Antipsychotics is risk factor Polycythaemia vera (raised RBC - hyperviscosity)
27
management ischaemic stroke <6hrs onset
1. Aspirin 300mg orally or rectally should be given as soon as possible if a hemorrhagic stroke has been excluded. Continue for 2 weeks. + Thrombolysis with alteplase if <4.5 hours since symptom onset + Thrombectomy if <6 hours (together with Thrombolysis with alteplase if <4.5 hours) and confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA
28
management of strokes presenting >6 hours after onset of symptoms
1. aspirin 300mg orally or rectally should be given as soon as possible if a hemorrhagic stroke has been excluded. Continue for 2 weeks. CT perfusion or diffusion-weighted MRI + thrombectomy if between 6 hours and 24 hours (including wake-up strokes) if there is the potential to salvage brain tissue, + consider if proximal posterior circulation
29
stroke patient. what do you do to manage complications and assess other aspects
DVT risk management: pressure stockings, IPCDs, not dalteparin as it could cause hemorrhagic transformation SALT referral for swallow screen - make nil by mouth in the meantime Disability is most commonly measured using the Barthel index (BI) ECG for ?AF If AF, 'anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days have passed from the onset of an ischaemic stroke'
30
when monitoring stroke pts what are important things to do?
24hr after thrombolysis do another CT to check you haven't caused haemorrhagic transformation Young person more likely to get raised ICP as their brain isn't atrophied so no space t swell - be alert for decrease in GCS
31
absolute contraindications to thrombolysis
- Previous intracranial haemorrhage - Seizure at onset of stroke - Intracranial neoplasm - Suspected subarachnoid haemorrhage - Stroke or traumatic brain injury in preceding 3 months - Lumbar puncture in preceding 7 days - Gastrointestinal haemorrhage in preceding 3 weeks - Active bleeding - Pregnancy - Oesophageal varices - Uncontrolled hypertension >200/120mmHg
32
pharmacological secondary prevention of stroke and TIA
1. Clopidogrel 2. Aspirin plus modified-release (MR) dipyridamole 3. MR dipyridamole if the cholesterol is > 3.5 mmol/l patients should be commenced on a statin. Atorvostatin 80mg. Many physicians will delay treatment until after at least 48 hours due to the risk of haemorrhagic transformation If AF, 'anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days have passed from the onset of an ischaemic stroke'
33
surgical considerations for secondary prevention of stroke/TIA
consider carotid artery endarterectomy: - if stroke/tia in carotid territory (eyes, ACA, MCA) and they are not severely disabled - should only be considered if carotid stenosis > 70% according ECST** criteria or > 50% according to NASCET*** criteria - Don’t operate on completely blocked as it is sealed so doesn’t embolize and cause strokes Don’t operate on a asymptomatic carotid
34
what are anterior circulation strokes? total vs partial
strokes involving the anterior cerebral artery / middle cerebral artery they cause: - Unilateral hemiparesis +/- hemisensory loss of 2 of: face, arm and leg - Homonymous hemianopia - High cognitive dysfunction eg dysphasia Total anterior circulation - all 3 of above criteria Partial anterior circulation - 2 of above criteria
35
how to differentiate between anterior cerebrala nd middle cerebrala rtery strokes
Anterior cerebral artery - contralateral hemiparesis + sensory loss (LL worse than UL) Middle cerebral artery - contralateral hemiparesis + sensory loss (UL worse than LL)
36
whata re posterior circualtion strokes? broad terms
Involve the vertebrobasilar (posterior cerebral, cerbellar arteries, basilar arteries) arteries and presents with one of: - Cerebellar or brainstem syndromes - Loss of consciousness - Isolated homonymous hemianopia
37
list the different types of posterior circulation stroke
- Posterior cerebral artery - Weber's syndrome (branch of PCA→ midbrain) - Anterior inferior cerebellar artery AICA (lateral pontine syndrome) - Posterior inferior cerebellar artery PICA (lateral medullary/wallenberg) - Basilar artery - Lacunar infarct
38
presentation posterior cerebral artery stroke
contralateral homonymous hemianopia with macular sparing with visual agnosia
39
presentation webers syndrome
ipsilateral CN 3 palsy, contralateral weakness of upper and lower extremity
40
presentation AICA
(lateral pontine syndrome) - ipsilateral facial paralysis, deafness, vertigo and vomiting
41
presentation PICA
(lateral medullary/wallenberg) - ipsilateral facial pain and temperature loss, contralateral limb/torso pain and temp loss, ataxia, nystagmus
42
presentation basilar artery stroke
locked in syndrome quadriplegia
43
presentation lacunar infarct
1 of: unilateral weakness of ⅔ of face,arm,leg(+/- sensory defecit), pure sensory stroke, ataxic hemiparesis. Often causes by HTN.
44
arteries/territories affected by lacunar infarct?
involves the perforating arteries around the internal capsule, thalamus and basal ganglia.
45
cause normally of alcunar infarct
HTN
46
Management ?TIA
immediate antithrombotic therapy - Give aspirin 300mg unless: --> pt has a blleeding disorder or taking anticoag (need CT to exclude ahemorrhage) --> pt already taking low dose aspirin (contnue current dose) --> aspirin contarindicated (discuss with specialist urgently) Specialist review - admit if crescenddo TIA or ?carotid stenosis or ?cardioembolic - within 24 hours if happene din past 7 days - within 1 week if symptoms were more than a week ago
47
when you have organised specialist review for TIA, what else do you need to advise the patient
Advise the person not to drive until they have been seen by a specialist
48
presentation of haemorrhagic stroke
Similar to ischaemic stroke or reduced consciousness Nausea Vomiting Headache Reduced GCS
49
causes of haemorrhagic stroke
Metastasis Vascular malformations (AVLs) Sinus venous thrombosis Hypertension (most common)
50
management of intracerebral haemorrhage
stop anticoagulants and antithombotics. consider reversal neurosurgical consult
51
name 4 stroke mimics
Hypoglycaemia Todd’s paresis Migraine Bell’s palsy
52
what is bells palsy
Bell's palsy may be defined as an acute, unilateral, idiopathic, facial nerve paralysis. The aetiology is unknown although the role of the herpes simplex virus has been investigated previously. The peak incidence is 20-40 years and the condition is more common in pregnant women.
53
forehead sparing means?
STROKE bells palsy has 5 branches so hand on face = it all so not forehead sparing lower motor neuron facial nerve palsy - forehead affected in contrast, an upper motor neuron lesion 'spares' the upper face patients may also notice post-auricular pain (may precede paralysis), altered taste, dry eyes, hyperacusis
54
management of bells palsy
1. Oral prednisolone within 72 hours of onset of Bell's palsy - seek specialist advice about use of antivirals
55
follow up bells palsy
if the paralysis shows no sign of improvement after 3 weeks, refer urgently to ENT a referral to plastic surgery may be appropriate for patients with more long-standing weakness e.g. several months
56
prognosis bells palsy
most people with Bell's palsy make a full recovery within 3-4 months if untreated around 15% of patients have permanent moderate to severe weakness
57
what is myasthenia gravis
Myasthenia gravis is an autoimmune disorder resulting in insufficient functioning acetylcholine receptors. Antibodies to acetylcholine receptors are seen in 85-90% of cases*. Myasthenia is more common in women (2:1)
58
key feature of myasthenia gravis
The key feature is muscle fatigability - muscles become progressively weaker during periods of activity and slowly improve after periods of rest: extraocular muscle weakness: diplopia proximal muscle weakness: face, neck, limb girdle ptosis dysphagia
59
symptoms myasthenia gravis
extraocular muscle weakness: diplopia proximal muscle weakness: face, neck, limb girdle ptosis dysphagia
60
what drugs may exacerbate myasthenia gravis
Beta-blockers — should be avoided if possible in patients with myasthenia gravis lithium phenytoin antibiotics: gentamicin, macrolides, quinolones, tetracyclines penicillamine quinidine, procainamide
61
investigations ?myasthenia gravis
AChR antibodies (acetylcholine receptor antibody) single fibre EMG (stimualtion of single fibres) high sensitivity (92-100%) CT thorax to exclude thymoma
62
management of myasthenia gravis
1. long-acting acetylcholinesterase inhibitors pyridostigmine is first-line (too tired to get to top of pyramid) + immunosuppression such as prednisolone + thymectomy
63
management of myastehnic crisis
- plasmapheresis - intravenous immunoglobulins
64
implications for anaesthesia myasthenia gravis
suxamethonium (muscle relaxant) normal doses won't work Suxamethonium is a depolarising NMBD - it acts by binding to and activating the receptor, at first causing muscle contraction, then paralysis. Due to a decreased number of available receptors, MG patients are typically resistant to depolarising NMBDs and may require significantly higher doses.
65
what drugs may cause proximal myopathy? will CK be raiseD?
statins - CK will be raised steroids - CK raised if acute, not raised if chronic
66
what is rhabdomyolysis
Rhabdomyolysis is caused by skeletal muscle breakdown. This causes the release of intracellular contents such as myoglobin and potassium into the blood stream. Excess myoglobin can precipitate in the glomerulus causing renal obstruction, direct nephrotoxicity and acute kidney injury.
67
triad rhabdomyolysis - symptoms
dark urine, generalised weakness and myalgia.
68
features of rhabdomyolysis blood tests etc.
acute kidney injury with disproportionately raised creatinine elevated creatine kinase (CK) myoglobinuria hypocalcaemia (myoglobin binds calcium) elevated phosphate (released from myocytes) hyperkalaemia (may develop before renal failure) metabolic acidosis
69
causes of rhabdomyolysis
seizure collapse/coma (e.g. elderly patients collapses at home, found 8 hours later) Ischaemia: embolism, surgery ecstasy crush injury McArdle's syndrome drugs: statins (especially if co-prescribed with clarithromycin)
70
diagnosis of rhabdomyolysis
A creatine kinase >5x the normal range is typically diagnostic.
71
management rhabdomyolysis
IV fluids to maintain good urine output Correction of electrolyte disturbances urinary alkalinization is sometimes used
72
electrolytes in rhabdomyolysis
Hyperkalaemia (liberated from the damaged muscle) Hyperphosphatemia (liberated from the damaged muscle) Hyperuricaemia (liberated from damaged muscle) Hypocalcaemia (calcium is taken into the damaged muscle by several mechanisms).
73
what endocrine things may cause proximal muscle weakness
cushings hypoadrenalism
74
what is muscualr dystrophy
umbrella term for genetic conditions that cause gradual weakening and wasting of muscles.
75
what pattern of weakness presents in muscualr dystrophy? what sign is this
Children with proximal muscle weakness use a specific technique to stand up from a lying position. This is called Gower’s sign. To stand up, they get onto their hands and knees, then push their hips up and backwards like the “downward dog” yoga pose. They then shift their weight backwards and transfer their hands to their knees. Whilst keeping their legs mostly straight they walk their hands up their legs to get their upper body erect. This is because the muscles around the pelvis are not strong enough to get their upper body erect without the help of their arms.
76
management muscualr dystrophy
Supportive Management is aimed at allowing the person to have the highest quality of life for the longest time possible. This usually involves input from occupational therapy, physiotherapy and medical appliances (such as wheelchairs and braces) as well as surgical and medical management of complications such as spinal scoliosis and heart failure.
77
genetics duchenne
defective gene for dystrophin on the X-chromosome X-linked recessive condition
78
if a mother is a carrier of defective dystrophin gene, what is the liklihood of her children being carriers/affected
50% chance of being a carrier if they are female and 50% chance of having the condition if they are male.
79
presentation duchenne
Boys with Duchenne's present around 3 – 5 years with weakness in the muscles around their pelvis. The weakness tends to be progressive and eventually all muscles will be affected. They are usually wheelchair bound by the time they become a teenager.
80
presentation beckers
The clinical course is less predictable than Duchennes. Symptoms only start to appear around 8 – 12 years. Some patients require wheelchairs in their late 20s or 30s . Others are able to walk with assistance into later adulthood. Management is similar to Duchennes.
81
genetics beckers
the dystrophin gene is less severely affected and maintains some of its function
82
key feature of myotonic dystrophy
Prolonged muscle contractions This may present in exams with a patient that is unable to let go after shaking someones hand, or unable to release their grip on a doorknob after opening a door. When doing an upper limb neurological examination always shake the patients hand and observe for difficulty releasing their grip.
83
how to determine where horners syndrome lesion is??
Horner's syndrome - anhydrosis determines site of lesion: head, arm, trunk = central lesion: stroke, syringomyelia 1st order just face = pre-ganglionic lesion: Pancoast's, cervical rib 2nd order absent = post-ganglionic lesion: carotid artery 3rd order imaging eye drops to determine site of lesion- apraclonidine to confirm horners followed by hydroxyamphetamine to determine site of lesion