Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Core clinical problems > 25. Weakness > Flashcards

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

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

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

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

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

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

causes of UMN lesions

A

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

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

LMN signs

A

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

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

test for conversion disorder weakness

A

hoovers sign

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

causes of peripheral muscle weakness? signs?

A

guillian barre
Charcot-marie tooth
lead poisoning

Ascending weakness
“Tripping over feet”
Foot drop
Hyporeflexia

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

causes of proximal muscle weakness

A

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

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

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

first line invetsigation ?inflammatory myopathy

A

creatinine kinase

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

invetsigations ?polymypositis/dermatomyositis

A

creatinine kinase

nerve conduction studies = Electromyography (EMG)

muscle biopsy for definitive

may want to look for underlying malignancy

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

define TIA

A

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what scoring sytem will you use when assessing ?stroke

A

ROSIER

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

first line for investigation ?stroke

A
  1. non contrast CT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

if a non-contrast CT shows ishcameic stroke/rules out haemorrhage, what other scans might you get?

A

CT angiography particularly if thrombectomy is being considered

MR angiography

CT perfusion scan or diffusion weighted MRI if looking for salvagable brain tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

risk factors for ischaemic stroke

A

OCP is a risk factor
Migraine is a risk factor
AF is a risk factor
Antipsychotics is risk factor
Polycythaemia vera (raised RBC - hyperviscosity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

management ischaemic stroke <6hrs onset

A
  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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

management of strokes presenting >6 hours after onset of symptoms

A
  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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

stroke patient. what do you do to manage complications and assess other aspects

A

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’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

when monitoring stroke pts what are important things to do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

absolute contraindications to thrombolysis

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

pharmacological secondary prevention of stroke and TIA

A
  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’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

surgical considerations for secondary prevention of stroke/TIA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are anterior circulation strokes? total vs partial

A

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
Q

how to differentiate between anterior cerebrala nd middle cerebrala rtery strokes

A

Anterior cerebral artery - contralateral hemiparesis + sensory loss (LL worse than UL)

Middle cerebral artery - contralateral hemiparesis + sensory loss (UL worse than LL)

36
Q

whata re posterior circualtion strokes? broad terms

A

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
Q

list the different types of posterior circulation stroke

A
  • 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
Q

presentation posterior cerebral artery stroke

A

contralateral homonymous hemianopia with macular sparing with visual agnosia

39
Q

presentation webers syndrome

A

ipsilateral CN 3 palsy, contralateral weakness of upper and lower extremity

40
Q

presentation AICA

A

(lateral pontine syndrome) - ipsilateral facial paralysis, deafness, vertigo and vomiting

41
Q

presentation PICA

A

(lateral medullary/wallenberg) - ipsilateral facial pain and temperature loss, contralateral limb/torso pain and temp loss, ataxia, nystagmus

42
Q

presentation basilar artery stroke

A

locked in syndrome
quadriplegia

43
Q

presentation lacunar infarct

A

1 of:

unilateral weakness of ⅔ of face,arm,leg(+/- sensory defecit),

pure sensory stroke,

ataxic hemiparesis. Often causes by HTN.

44
Q

arteries/territories affected by lacunar infarct?

A

involves the perforating arteries around the internal capsule, thalamus and basal ganglia.

45
Q

cause normally of alcunar infarct

A

HTN

46
Q

Management ?TIA

A

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
Q

when you have organised specialist review for TIA, what else do you need to advise the patient

A

Advise the person not to drive until they have been seen by a specialist

48
Q

presentation of haemorrhagic stroke

A

Similar to ischaemic stroke or reduced consciousness
Nausea
Vomiting
Headache
Reduced GCS

49
Q

causes of haemorrhagic stroke

A

Metastasis
Vascular malformations (AVLs)
Sinus venous thrombosis
Hypertension (most common)

50
Q

management of intracerebral haemorrhage

A

stop anticoagulants and antithombotics. consider reversal

neurosurgical consult

51
Q

name 4 stroke mimics

A

Hypoglycaemia
Todd’s paresis
Migraine
Bell’s palsy

52
Q

what is bells palsy

A

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
Q

forehead sparing means?

A

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
Q

management of bells palsy

A
  1. Oral prednisolone within 72 hours of onset of Bell’s palsy
  • seek specialist advice about use of antivirals
55
Q

follow up bells palsy

A

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
Q

prognosis bells palsy

A

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
Q

what is myasthenia gravis

A

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
Q

key feature of myasthenia gravis

A

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
Q

symptoms myasthenia gravis

A

extraocular muscle weakness: diplopia
proximal muscle weakness: face, neck, limb girdle
ptosis
dysphagia

60
Q

what drugs may exacerbate myasthenia gravis

A

Beta-blockers — should be avoided if possible in patients with myasthenia gravis

lithium
phenytoin
antibiotics: gentamicin, macrolides, quinolones, tetracyclines
penicillamine
quinidine, procainamide

61
Q

investigations ?myasthenia gravis

A

AChR antibodies (acetylcholine receptor antibody)
single fibre EMG (stimualtion of single fibres) high sensitivity (92-100%)

CT thorax to exclude thymoma

62
Q

management of myasthenia gravis

A
  1. long-acting acetylcholinesterase inhibitors
    pyridostigmine is first-line

(too tired to get to top of pyramid)

+ immunosuppression such as prednisolone
+ thymectomy

63
Q

management of myastehnic crisis

A
  • plasmapheresis
  • intravenous immunoglobulins
64
Q

implications for anaesthesia myasthenia gravis

A

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
Q

what drugs may cause proximal myopathy? will CK be raiseD?

A

statins - CK will be raised

steroids - CK raised if acute, not raised if chronic

66
Q

what is rhabdomyolysis

A

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
Q

triad rhabdomyolysis - symptoms

A

dark urine, generalised weakness and myalgia.

68
Q

features of rhabdomyolysis blood tests etc.

A

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
Q

causes of rhabdomyolysis

A

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
Q

diagnosis of rhabdomyolysis

A

A creatine kinase >5x the normal range is typically diagnostic.

71
Q

management rhabdomyolysis

A

IV fluids to maintain good urine output

Correction of electrolyte disturbances

urinary alkalinization is sometimes used

72
Q

electrolytes in rhabdomyolysis

A

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
Q

what endocrine things may cause proximal muscle weakness

A

cushings

hypoadrenalism

74
Q

what is muscualr dystrophy

A

umbrella term for genetic conditions that cause gradual weakening and wasting of muscles.

75
Q

what pattern of weakness presents in muscualr dystrophy? what sign is this

A

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
Q

management muscualr dystrophy

A

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
Q

genetics duchenne

A

defective gene for dystrophin on the X-chromosome

X-linked recessive condition

78
Q

if a mother is a carrier of defective dystrophin gene, what is the liklihood of her children being carriers/affected

A

50% chance of being a carrier if they are female

and 50% chance of having the condition if they are male.

79
Q

presentation duchenne

A

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
Q

presentation beckers

A

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
Q

genetics beckers

A

the dystrophin gene is less severely affected and maintains some of its function

82
Q

key feature of myotonic dystrophy

A

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
Q

how to determine where horners syndrome lesion is??

A

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

Core clinical problems (94 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions