Limb weakness Flashcards
1
Q
What things might get confused with limb weakness?
A
- Limb ataxia
- Limb numbness (reduced sensation)
- Limb pain - too painful to move
2
Q
What are the time courses for the onset of limb weakness and suggest how this could reflect the potential pathologies?
A
- Sudden onset (seconds to minutes) - suggests traumatic (e.g. displaced vertebral fractures) or vascular insults (e.g. stroke, TIA)
- Subacute onset (hours to days) - progressive demyelination (Guilla-Barre or MS) or a slowly expanding haematoma
- Chronic onset (weeks to months) - slow growing tumour or motor neurone disease
3
Q
Outline the neuro-anatomical pathway from the motor cortex all the way down to the muscle cells
A
- M1 (primary motor cortex)
- Corona radiata
- Internal capsule
- Pons (via cerebral peduncles)
- Medulla - point of decussation for 90% of fibres
- Down the spinal cord in the corticospinal tract
- Nerve roots and plexus
- Neuromuscular junction
- Muscle
4
Q
DDx (see notes)
A
5
Q
What things are important to elicit from a neurological history in someone with limb weakness, and why?
A
- Time / onset?
- Visual / speech disturbance?
- Indicates central disturbance rather than spinal cord or periphal nerves
- Headache?
- Unusual in vascular causes - stroke or TIA
- Sudden-onset, terrible headache - subarachnoid haemorrhage
- Unilateral headache preceding limb weakness - hemiplegic migraine
- Gradual-onset headache preceding limb weakness - intracranial mass such as slowly expanding subdural haemorrhage
- Seizure or loss of consciousness?
- Not typical of stroke
- Todd’s paresis (post-seizure) stroke mimic
- Hypoglycaemia
- Neck or back pain?
- Suspect spinal pathology such as…
- Spontaneous disc prolapse
- Traumatic injury to the spine
- Discitis
- Spinal abscess
- OR Guillan-Barre
- Head Trauma?
- Subdural haemorrhages - including slowly expanding subdural haemorrhages in elderly patients
- Risk factors for stroke?
- Previous stroke / TIA
- AF
- Atherosclerotic risk factors
- Migraine with aura
- SLE
6
Q
Outline the different UMN and LMN signs
A
UMN
- ↑ Tone
- ↑ Reflexes
- ↑ Plantars (Babinski’s reflex)
- Clonus (sometimes)
HOWEVER, important to note that the acute phase of UMN pathologies cause hypotonia and hyporeflexia, as in LMN pathologies, and only then do they progress to hypertonia and hyperreflexia
LMN
- ↓ Tone
- ↓ Reflexes
- Fasciculations (sometimes)
- Wasting
7
Q
1) The presence of language defects suggests pathology in which general region?
2) What are the 2 types of language defects - describe these and identify which specific area of the brain is affected?
A
1)
- Cortex of the dominant hemisphere (usually left, even in left handed people)
2)
- Receptive (Wernicke’s) dysphagia - the patient speaks fluently (although with jumbled words / phrases) but cannot comprehend language
- Lesion in Wernicke’s area (in the temporal lobe) of the dominant hemisphere
- Expressive (Broca’s) dysphagia - the patient can comprehend language and follow instructions, but cannot find words or speak fluently
- Lesion in Broca’s area (in the frontal lobe) of the dominant hemisphere
*
8
Q
Describe what occurs in attention defects and where these localise pathologies to
A
- Patient appears to be ignoring half of their sensory world (e.g. responding only to cues on one side of the bed)
- Parietal cortex lesion
9
Q
Outline the neuroanatomy for vision (also draw this out)
A
- Retina
- Nerve fibres from nasal and temporal aspects of each eye
- These converge at the optic nerve
- Most fibres decussate at the optic chiasm, however some remain ipsilateral
- Then down via optic tracts
- To the LGN (Lateral Geniculate Nucleus)
- Optic radiations
- Occipital lobe
10
Q
Where is the lesion in a patient with complete blindness in one eye in terms of neural visual field defects?
A
- Optic nerve
11
Q
Where is the lesion in a patient with homonymous hemianopia in terms of neural visual field defects?
A
- In the ipsilateral optic tract OR
- The contralateral occipital lobe
12
Q
Where is the lesion in a patient with bitemporal hemianopia?
A
- Optic chiasm
13
Q
If there is eye deviation in the context of limb weakness
1) Towards the weak limb
2) Away from the weak limb
What does this suggest in terms of localisation of the lesion?
A
1)
- Cortical lesion
2)
- Brain-stem lesion
14
Q
How can sensory signs help diagnosis in LMN and UMN lesions?
A
LMN
- Nerve root / peripheral nerve lesion - sensory signs present
- Neuromuscular / muscular lesion - sensory signs absent
UMN
- Damage to specific spinal cord tracts
- Spinothalamic (pain and temperature paraesthesia)
- Dorsal column (light touch, vibration, position sense or proprioception paraesthesia)
- Therefore, for example anterior spinal artery infarct spares the dorsal column so these sensory modalities are spared
15
Q
What does the following suggest, facial nerve palsy and
1) Forehead involvement and bilateral blinking problems?
2) Forehead sparing and no bilateral blinking problems?
A
1)
- LMN lesion - final common pathway to the frontalis and orbicularis muscle is destroyed
- OR bilateral UMN lesion?
2)
- Unilateral UMN lesion
16
Q
1) Based on the motor homunculus, what would stroke in the anterior cerebral artery and middle cerebral artery cause?
2) Also what else would infarct of the middle cerebral artery (MCA) cause based on it supplying another neuroanatomical structure - and what is this structure?
A
1)
- Anterior cerebral artery supplies the medial M1 and therefore based on the motor homunculus might affect the lower limb
- Middle cerebral artery - lateral M1 and therefore, based on teh motor homunculus, might affect the thorax all the way up to the face, tongue and pharynx as you go more lateral
2)
- Supplies the right posterior parietal cortex, where damage can cause contralateral hemineglect
17
Q
Why are carotid bruits of interest in a limb weakness picture?
A
- Carotid bruits could be due to aortic stenosis OR carotid artery atheromas
- Emboli point to vascular causes such as TIA or stroke
18
Q
1) Define TIA
2) Define stroke
A
- Define TIA - occlusion of a cerebral artery / arteriole that has fully resolved within 24hrs, without leaving any infarcted
- Define stroke - occlusion of a cerebral artery / arteriole lasting >24hrs, leaving behind infarcted tissue
19
Q
What first-line investigations must be arranged after you suspect stroke (upon making a clinical diagnosis - i.e. based upon history and examination)?
A
- CT head - can also pick up fresh blood well in haemorrhages, although signs of infarction may take up to 24hrs to become apparent. Helps identify if the stroke was ischaemic or haemorrhagic in nature among other uses
- FBC - may reveal cause of occlusion
- Polycythaemia
- Thrombocytosis
- Haemorrhage (e.g. thrombocytopenia)
- Blood glucose - exclude hypoglycaemia as the cause of limb weakness (alongside the stroke)
- Blood clotting - exclude haemophilia, coagulopathy etc and especially important in patients taking warfarin
- ECG - AF as a cause of embolisation
20
Q
1) What are the 2 pathophysiological (not anatomical) classifications of stroke?
2) Why is it important to determine which one is the cause?
A
1)
- Ischaemic
- Haemorrhagic
2)
- Ischaemic stroke is treated using thrombolysis (e.g. tPA) + anti-platelet therapy
- If these are used in haemorrhagic stroke, it will worsen it
21
Q
What is the management plan for ischaemic stroke?
A
- Thrombolysis (if within 4.5hrs) - e.g. tPA (tissue plasminogen activator)
- Anti-platelets (e.g. aspirin
- Stroke-unit / specialist ward referral
- VTE prophylaxis
22
Q
What second line investigations are there after you suspect ischaemic stroke in a patient (upon having made a clinical diagnosis - i.e. from the diagnosis and examination)?
A
- Carotid artery doppler u/s - identifies any carotid artery stenosis due to carotid artery atheromas which could be the cause behind the ischaemic stroke, and also could be a candidate for removal by carotid endarterectomy by vascular surgeons
- Echocardiogram
- Identifies cardiac sources of emboli - atrial thrombus (indicated by AF, recent MI, abnormla ECG, heart murmur, ischaemic events affecting more than one cerebral artery territory
- Identifies any patent foramen ovale
23
Q
Complications of ischaemic stroke?
A
- Pressure ulcers (bedsores)
- Aspiration pneumonia (due to difficulties swallowing)
- VTE and recurrent ischaemic stroke
24
Q
What is the management for TIA?
A
25
What are the 2 types of emboli that cause ischaemic stroke and what are the best treatments for these?
* 'Red emboli' - clots forming through blood stasis - in deep veins or fibrillating atria (in AF) - rich in firbrin and erythrocytes - responsive to anticoagulants that inhibit fibrin formation
* Warfarin and rivaroxaban
* 'White emboli' - clots that form through endothelial activation of plaques (such as those that form upon atherosclerotic plaque rupture)
* Antiplatelets - aspirin 300mg, clopidogrel
N.B. therefore aspirin is not given in patients who had an ischaemic stroke due to atrial fibrillation causing the initial clot which then embolised - it would be pointless
26
In cord compression
1) What is the pattern of signs?
2) What are the causes?
3) What is the first investigation that you should do?
1)
* UMN signs (e.g. hypertonia, hyperflexia and clonus etc) - so can localise to either brain or spine
* But also signs below a certain level e.g. loss of sensation below umbilicus - indicates spinal localisation
2)
* Disc herniation
* Spondylolisthesis
* Space-occupying lesion
* Tumour
* Abscess
* Cyst
* Haematoma
3)
* Spinal MRI - to identify the cause behind the cord compression - e.g. will find any space-occupying lesion
27
If you get UMN signs - thereby indicating a lesion in either the brain or the spine, what is there about the pattern of limb weakness that could indicate it is one of these?
* Bilateral limb weakess is unlikely to be due to lesions in the brain since you would need lesions in both hemispheres - unlikely
* Therefore it is more likely to be in the spinal cord
28
What are the signs and symptoms that MS can have?
* Spastic (UMN signs) paraparesis - MS is a UMN disease
* Optic neuritis (painful eye with blurred vision that spontaneously resolves after a week or so)
* INO (internuclear opthalmoplegia)
* So, multiple lesions at different times over a period of years or months are consistent with a demyelinating disorder - hence the visual and motor disturbances that can appear at different times
* AND in particular there is strong association with optic neuritis and INO
* RAPD defects may also be present in the eye affected by the optic neuritis
29
What investigations must be carried out if you suspect MS?
* LP (Lumbar Puncture) - look for oligoclonal bands (raised levels of multiple IgG antibodies in CSF)
* MRI of brain and spinal cord - look for sclerotic (de-myelinated) plaques
* Visually evoked potentials - optic neuritis causes demyelination of the optic nerve (thereby reducing speed of conduction) - this test can indicate the speed of conduction down the optic nerve by deduction from the time a visual stimulus is displayed to activation of visual cortices
30
What is Brown-sequard and explain its features anatomically?
* Hemisection of the spinal cord
* Motor neurones decussate at the medulla and therefore once they are in the spinal cord, they then continue ipsilaterally and then eventually innervate skeletal muscle **ipsilaterally** as far as the spinal cord is concerned
* Therefore there is paralysis on the side of the lesion
* Dorsal column neurones (vibration, proprioception, fine touch) also decussate at the level of medulla (at the medial lemniscus) and from there, continue **ipsilaterally** in the spinal cord
* Therefore there is loss of vibration, proprioception and fine touch at the side of the lesion)
* Spinothalamic neurones (decussate at the level of what they innervate i think?) so they innervate the **contralateral** side of the body
* Therefore there is contralateral loss of pain and temperature sensation
31
What is the grading scale used to grade limb weakness and what are the different levels?
* Grade 5 - Normal power
* Grade 4 - Can move limb against gravity and some resistance exerted by examiner
* Grade 3 - Can move limbs against gravity
* Grade 2 - Movement only if gravity is eliminated
* Grade 1 - Flicker is perciptible in muscle
* Grade 0 - No movement
32
What do the following prefixes mean...?
1) Mono-
2) Hemi-
3) Para-
4) Tetra- / quadra-
What do the following suffixes mean...?
5) -paresis
6) -plegia
1)
* One-limb
2)
* One-side of the body
3)
* Lower limbs
4)
* All four limbs
5)
* Limb weakness
6)
* Complete paralysis
33
What is the site of the lesion in full body hemiparesis?
* Contralateral cerebral motor cortex (e.g. widespread stroke)
* Contralateral corona radiata (e.g. stroke)
* Contralateral internal capsule (e.g. stroke)
* Contralateral pons (e.g. stroke)
34
Where is the site of the lesion in limb hemiparesis, and what is the difference between full bodyhemiparesis and limb hemiparesis?
* Contralateral cerebral motor cortex (e.g. stroke)
* Contralateral corona radiata (e.g. stroke)
* Contralateral internal capsule (e.g. stroke)
* Contralateral pons (e.g. stroke)
* Ipsilateral spinal lateral motor tract (e.g. cervical disc prolapse
* Full body hemiparesis includes the face, whereas limb hemiparesis does not
35
Where is the site of the lesion in isolated limb weakness?
* Contralateral cerebral motor cortex (e.g. stroke)
* Contralateral corona radiata (e.g. stroke)
* Contralateral internal capsule (e.g. stroke)
* Contralateral pons (e.g. stroke)
* Ipsilateral peripheral nerve root (e.g. osteophyte)
* Ipsilateral peripheral nerve plexus (e.g. trauma to brachial plexus)
* Ipsilateral peripheral nerve *per se* (angiogram sheath injury to femoral nerve)
36
Where is the site of the lesion in paraparesis?
* Bilateral cerebral motor cortex (e.g. parasagittal meningioma)
* Bilateral motor spinal tracts (e.g. cord compression)
* Cauda equina (e.g. lumbar intervertebral disc prolapse)
* Bilateral lumbosacral plexus (e.g. Guillan-Barre syndrome)
37
Where is the site of the lesion in tetraplegia?
* Bilateral motor tracts of cervical spinal cord (e.g. traumatic spinal cord transection at C5)
* Peripheral nerves (demyelinating disease i.e Guillan-Barre syndrome)
38
Where is the site of the lesion in proximal muscle weakness?
* NMJ junction (e.g. myasthenia gravis, Eaton-Lambert syndrome)
* Muscle (e.g. polymyositis, dermatomyositis) or secondary to other conditions (e.g. hyperparathyroidism) or drugs (e.g. statins)
39
Where is the site of the lesion when there are several episodes separated in time and space?
* Various sites in CNS (e.g. MS)
40
Which nerve roots are tested in the following reflexes?
1) Ankle jerk
2) Knee jerk
3) Biceps reflex
4) Triceps reflex
1)
* S1 / S2
2)
* L3 / L4
3)
* C5 / C6
4)
* C7 / C8
41
True or false, hypoglycaemia causing limb weakness usually resolves within 1 hr
FALSE
42
1) Migraine and epilepsy can cause limb weakness. What signs and symptoms can you get in these (that you also don't get in TIA)?
2) How can you differentiate between migraine and epilepsy as causes?
1)
* Positive symptoms
* Tingling
* Shaking
* Vision disturbances - you get wiggly lines in your vision in migrain with aura and sometimes in epilepsy
* (Unlike loss of function in TIAs)
2)
* Migraines have auras that evolve over 20-30 minutes (i.e. long time)
* Also you can get headaches as well (but not always)
* Whereas the onset of epilepsy is very sudden
43
General revision prompt - revise dermatomes and nerve supplying different parts of arms and hands and legs and feet - motor and sensory supply
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